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1. Lamant L, de Reyniès A, Duplantier MM, Rickman DS, Sabourdy F, Giuriato S, Brugières L, Gaulard P, Espinos E, Delsol G: Gene-expression profiling of systemic anaplastic large-cell lymphoma reveals differences based on ALK status and two distinct morphologic ALK+ subtypes. Blood; 2007 Mar 1;109(5):2156-64
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gene-expression profiling of systemic anaplastic large-cell lymphoma reveals differences based on ALK status and two distinct morphologic ALK+ subtypes.
  • With the use of microarray gene-expression profiling, we analyzed a homogeneous series of 32 patients with systemic anaplastic large-cell lymphoma (ALCL) and 5 ALCL cell lines.
  • Unsupervised analysis classified ALCL in 2 clusters, corresponding essentially to morphologic subgroups (ie, common type vs small cell and "mixed" variants) and clinical variables.
  • Patients with a morphologic variant of ALCL had advanced-stage disease.
  • Supervised analysis showed that ALK+ALCL and ALK- ALCL have different gene-expression profiles, further confirming that they are different entities.
  • Among the most significantly differentially expressed genes between ALK+ and ALK- samples, we found BCL6, PTPN12, CEBPB, and SERPINA1 genes to be overexpressed in ALK+ ALCL.
  • The molecular signature of ALK- ALCL included overexpression of CCR7, CNTFR, IL22, and IL21 genes but did not provide any obvious clues to the molecular mechanism underlying this tumor subtype.
  • Once confirmed on a larger number of patients, the results of the present study could be used for clinical and therapeutic management of patients at the time of diagnosis.
  • [MeSH-major] Cell Shape. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Lymphoma, Large-Cell, Anaplastic / genetics. Lymphoma, Large-Cell, Anaplastic / pathology. Protein-Tyrosine Kinases / genetics
  • [MeSH-minor] Cell Line, Tumor. Humans. Immunohistochemistry. RNA, Messenger / genetics. Receptor Protein-Tyrosine Kinases. Tissue Array Analysis


2. Park SR, Baek JY, Kim DW, Im SA, Kim TY, Bang YJ, Kim NK, Jeon YK, Kim CW, Heo DS: Primary systemic anaplastic large cell lymphoma in a single Korean institution: clinical characteristics and treatment outcome. J Korean Med Sci; 2006 Aug;21(4):633-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary systemic anaplastic large cell lymphoma in a single Korean institution: clinical characteristics and treatment outcome.
  • Despite advances in the characterization of anaplastic large cell lymphoma (ALCL), little data is available on Asian patients.
  • We report here upon single Korean institution's experience regarding the clinical characteristics and outcomes of ALCL.
  • We performed a retrospective study of 32 adults with ALCL.
  • Ann Arbor stage III-IV, B symptoms, high-intermediate/ high International Prognostic Index (IPI), and extranodal disease at diagnosis were present in 56%, 44%, 41%, and 63%, respectively.
  • The staining results for anaplastic lymphoma kinase were positive in 6 (33%) of 18 cases available.
  • Age, performance status, lactate dehydrogenase, extranodal disease sites number, and IPI were correlated with treatment response and survival.
  • Our data suggest that Korean ALCL patients appear to have a higher male/female ratio, less frequent skin/bone involvement, and lower CR rate compared with those of Western studies.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / drug therapy. Lymphoma, Large-Cell, Anaplastic / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Antigens, CD30 / analysis. Female. Humans. Korea. Male. Middle Aged. Neoplasm Recurrence, Local. Neoplasm Staging. Prognosis. Retrospective Studies. Survival Analysis. Treatment Outcome

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  • (PMID = 16891805.001).
  • [ISSN] 1011-8934
  • [Journal-full-title] Journal of Korean medical science
  • [ISO-abbreviation] J. Korean Med. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Antigens, CD30
  • [Other-IDs] NLM/ PMC2729883
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3. Park SJ, Kim S, Lee DH, Jeong YP, Bae Y, Han EM, Huh J, Suh C: Primary systemic anaplastic large cell lymphoma in Korean adults: 11 years' experience at Asan Medical Center. Yonsei Med J; 2008 Aug 30;49(4):601-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary systemic anaplastic large cell lymphoma in Korean adults: 11 years' experience at Asan Medical Center.
  • PURPOSE: Anaplastic large cell lymphoma (ALCL), a CD30+ T-cell non-Hodgkin's lymphoma, represents only 2-8% of lymphoma overall.
  • Information on the clinical findings of primary systemic ALCL in Korea is limited.
  • Our aims were to report the clinical features and outcomes of primary systemic ALCL.
  • PATIENTS AND METHODS: We retrospectively reviewed the medical records of 36 adult patients diagnosed with primary systemic ALCL at Asan Medical Center from February 1995 through June 2006.
  • Univariate analysis showed that performance status (p = 0.035), international prognostic index (IPI) (p = 0.025), and age-adjusted IPI (p = 0.034) were significant prognostic factors for OS, whereas anaplastic lymphoma kinase (ALK) expression did not affect OS (p = 0.483).
  • CONCLUSION: Our retrospective analysis of Korean primary systemic ALCL patients showed that median OS was 49 months and overall response to CHOP was 91%.
  • [MeSH-major] Hospitals. Lymphoma, Large-Cell, Anaplastic / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Disease-Free Survival. Female. Humans. Korea / epidemiology. Male. Middle Aged. Neoplasm Staging. Protein-Tyrosine Kinases / metabolism. Receptor Protein-Tyrosine Kinases. Survival Rate. Time Factors

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  • (PMID = 18729302.001).
  • [ISSN] 0513-5796
  • [Journal-full-title] Yonsei medical journal
  • [ISO-abbreviation] Yonsei Med. J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Other-IDs] NLM/ PMC2615286
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4. Querfeld C, Khan I, Mahon B, Nelson BP, Rosen ST, Evens AM: Primary cutaneous and systemic anaplastic large cell lymphoma: clinicopathologic aspects and therapeutic options. Oncology (Williston Park); 2010 Jun;24(7):574-87
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary cutaneous and systemic anaplastic large cell lymphoma: clinicopathologic aspects and therapeutic options.
  • Anaplastic large cell lymphoma (ALCL) is a biologic and clinically heterogenous subtype of T-cell lymphoma.
  • Clinically, ALCL may present as localized (primary) cutaneous disease or widespread systemic disease.
  • These two forms of ALCL are distinct entities with different clinical and biologic features.
  • Both types share similar histology, however, with cohesive sheets of large lymphoid cells expressing the Ki-1 (CD30) molecule.
  • Primary cutaneous ALCL (C-ALCL) is part of the spectrum of CD30+ lymphoproliferative diseases of the skin including lymphomatoid papulosis.
  • Using conservative measures, 5-year disease-free survival rates are > 90%.
  • The systemic ALCL type is an aggressive lymphoma that may secondarily involve the skin, in addition to other extranodal sites.
  • Further, systemic ALCL may be divided based on the expression of anaplastic lymphoma kinase (ALK) protein, which is activated most frequently through the nonrandom t(2;5) chromosome translocation, causing the fusion of the nucleophosmin (NPM) gene located at 5q35 to 2p23 encoding the receptor tyrosine kinase ALK.
  • Systemic ALK+ ALCLs have improved prognosis compared with ALK-negative ALCL, although both subtypes warrant treatment with polychemotherapy.
  • Allogeneic and, to a lesser extent, autologous stem cell transplantation play a role in relapsed disease, while the benefit of upfront transplant is not clearly defined.
  • In addition, a multitude of novel therapeutics are being studied, including anti-CD30 antibodies, histone deacetylase inhibitors, immunomodulatory drugs, proteasome inhibitors, and inhibitors of ALK and its downstream signaling pathways.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / pathology. Lymphoma, Large-Cell, Anaplastic / therapy. Lymphoma, Primary Cutaneous Anaplastic Large Cell / pathology. Lymphoma, Primary Cutaneous Anaplastic Large Cell / therapy. Skin Neoplasms / pathology. Skin Neoplasms / therapy
  • [MeSH-minor] Antigens, CD30 / physiology. Humans. Immunophenotyping

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  • [CommentIn] Oncology (Williston Park). 2010 Jun;24(7):587, 592-3 [20669795.001]
  • [CommentIn] Oncology (Williston Park). 2010 Jun;24(7):594 [20669796.001]
  • (PMID = 20669794.001).
  • [ISSN] 0890-9091
  • [Journal-full-title] Oncology (Williston Park, N.Y.)
  • [ISO-abbreviation] Oncology (Williston Park, N.Y.)
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD30
  • [Number-of-references] 118
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5. Wang FH, Li YH, Zeng J, Rao HL, Xia ZJ, Sun XF, Huang HQ, Lin TY, Jiang WQ, Guan ZZ: Clinical analysis of primary systemic anaplastic large cell lymphoma: a report of 57 cases. Ai Zheng; 2009 Jan;28(1):49-53
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical analysis of primary systemic anaplastic large cell lymphoma: a report of 57 cases.
  • BACKGROUND AND OBJECTIVE: The clinical characteristics and prognosis of primary systemic anaplastic large cell lymphoma (ALCL) are various according to different reports.
  • Anaplastic lymphoma kinase (ALK), a specific marker of primary systemic ALCL, is related with its clinical characteristics and prognosis.
  • This study was to investigate the clinical characteristics and prognosis of primary systemic ALCL, and to explore the expression and clinical significance of ALK.
  • METHODS: Clinical data of 57 primary systemic ALCL patients, treated in Cancer Center of Sun Yat-sen University from January 1997 to January 2006, were reviewed.
  • Of the 57 patients, 33 (57.9%) had B symptoms, 23 (40.4%) had Ann Arbor stage III-IV tumors, and 23 (40.4%) had extranodal disease at diagnosis.
  • The positive rate of ALK was 63.0% in the 46 cases detected.
  • Compared with ALK-negative patients, ALK-positive patients were younger (p = 0.001) and had higher expected 5-year survival rate (p < 0.01).
  • Multivariate analysis confirmed the independent prognostic values of ALK expression, primary disease site and lactate dehydrogenase (LDH) level.
  • CONCLUSIONS: Primary systemic ALCL usually occurs in young patients, with good response to chemotherapy and good prognosis.
  • No ALK expression, high-intermediate/high IPI, extranodal disease and elevated LDH level are correlated to unfavorable prognosis.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / drug therapy. Protein-Tyrosine Kinases / analysis

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  • (PMID = 19448428.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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6. Shi YF, Liu CL, Zhou CJ, Gong LP, Dong LN, Li M, Huang X, Gao ZF: [Anaplastic lymphoma kinase gene abnormality and the expression of its fusion protein in primary systemic anaplastic large cell lymphoma]. Beijing Da Xue Xue Bao; 2008 Aug 18;40(4):380-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Anaplastic lymphoma kinase gene abnormality and the expression of its fusion protein in primary systemic anaplastic large cell lymphoma].
  • OBJECTIVE: To study the expression of anaplastic lymphoma kinase (ALK) and chromosome breakage of the anaplastic lymphoma kinase (ALK) gene retrospectively and to investigate their possible value as indicators of prognosis in primary systemic anaplastic large cell lymphomas (S-ALCL).
  • METHODS: Twenty-eight cases of S-ALCL were collected from the Lymphoma Lab, the Department of Pathology, Peking University Health Science Center and Beijing Children's Hospital.
  • The morphologic characteristics were studied under light microscope, and essential immunohistochemical staininings (IHC) were performed and reviewed to confirm the diagnosis of S-ALCL.
  • Locus specific interphase fluorescence in situ hybridization (LSI-FISH) was also performed on the neoplastic cells using paraffin-embedded tissues to detect ALK gene abnormality.
  • In 14 ALCL cases, ALK gene breakage was detected by LSI-FISH, using a dual-color break-apart ALK gene DNA (LSI-ALK) probe.
  • CONCLUSION: IHC detection for ALK fusion protein is important to the diagnosis of S-ALCL.
  • Complex abnormalities of ALK gene exist in S-ALCL cases, and different types of ALK gene might lead to different clinical outcome.
  • [MeSH-major] Chromosome Breakage. Lymphoma, Large-Cell, Anaplastic / genetics. Protein-Tyrosine Kinases / genetics

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  • (PMID = 18677384.001).
  • [ISSN] 1671-167X
  • [Journal-full-title] Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences
  • [ISO-abbreviation] Beijing Da Xue Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Recombinant Fusion Proteins; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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7. Kitamura N, Katagiri YU, Itagaki M, Miyagawa Y, Onda K, Okita H, Mori A, Fujimoto J, Kiyokawa N: The expression of granulysin in systemic anaplastic large cell lymphoma in childhood. Leuk Res; 2009 Jul;33(7):908-12
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  • [Title] The expression of granulysin in systemic anaplastic large cell lymphoma in childhood.
  • The expression of granulysin, a cytolytic protein produced by activated T and NK cells, has been revealed to be correlated with the prognosis of some adult cancer patients.
  • By examination on various childhood lymphoma tissues, we found that granulysin level was especially high in systemic anaplastic large cell lymphoma (ALCL) cases, whereas no close correlation with the expression of CD96, a marker for activated T and NK cells, was observed.
  • We further demonstrated that both ALCL cells in biopsy specimens and cell lines established from ALCL express granulysin, indicating some correlation of granulysin with biological features of ALCL.
  • [MeSH-major] Antigens, Differentiation, T-Lymphocyte / genetics. Burkitt Lymphoma / genetics. Hodgkin Disease / genetics. Lymphoma, B-Cell / genetics. Lymphoma, Large B-Cell, Diffuse / genetics. Lymphoma, Large-Cell, Anaplastic / genetics. RNA, Messenger / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Antigens, CD / genetics. Antigens, CD / metabolism. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Female. Flow Cytometry. Humans. Killer Cells, Natural / metabolism. Killer Cells, Natural / pathology. Male. Middle Aged. Prognosis. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured. Young Adult

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  • (PMID = 19243819.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Differentiation, T-Lymphocyte; 0 / Biomarkers, Tumor; 0 / CD96 antigen; 0 / GNLY protein, human; 0 / RNA, Messenger
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8. Kaliyadan F, Ray S, Mathew MK, Pai S, Sasikala L, Pai R: A rapidly progressing, fatal case of primary systemic anaplastic large cell lymphoma presenting as erythroderma--association with carbamazepine. Dermatol Online J; 2008;14(12):5
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  • [Title] A rapidly progressing, fatal case of primary systemic anaplastic large cell lymphoma presenting as erythroderma--association with carbamazepine.
  • A 73-year-old male patient admitted with erythroderma was diagnosed to have primary systemic Analpastic Lymphoma Kinase (ALK) positive, CD 30 positive, anaplastic large cell lymphoma.
  • The patient's condition deteriorated rapidly during the period after the diagnosis was confirmed, with subsequent death before chemotherapy could be started.
  • Here we highlight the possibility of carbamazepine inducing anaplastic large cell lymphomas and the need for a high level of suspicion to make an early diagnosis allowing rapid appropriate treatment in such cases.
  • [MeSH-major] Carbamazepine / adverse effects. Dermatitis, Exfoliative / complications. Lymphoma, Large-Cell, Anaplastic / diagnosis. Lymphoma, Large-Cell, Anaplastic / etiology
  • [MeSH-minor] Aged. Diabetic Neuropathies / drug therapy. Disease Progression. Fatal Outcome. Humans. Male. Tomography, X-Ray Computed

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  • (PMID = 19265618.001).
  • [ISSN] 1087-2108
  • [Journal-full-title] Dermatology online journal
  • [ISO-abbreviation] Dermatol. Online J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 33CM23913M / Carbamazepine
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9. Shi Y, Chen G, Zhou XG, Gong LP, Yu R, Zheng YY, Xie JL, Jin Y: [Clinicopathologic features of 66 cases of anaplastic lymphoma kinase positive and negative systemic anaplastic large cell lymphoma: a comparative study]. Zhonghua Bing Li Xue Za Zhi; 2010 Apr;39(4):235-9
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  • [Title] [Clinicopathologic features of 66 cases of anaplastic lymphoma kinase positive and negative systemic anaplastic large cell lymphoma: a comparative study].
  • OBJECTIVE: To study the clinicopathologic features of 66 cases of primary systemic anaplastic large cell lymphoma (ALCL), with emphasis on the differences between ALK-positive and ALK-negative cases.
  • METHODS: The clinical data of 66 cases of ALCL was analyzed.
  • Immunohistochemical study for CD30, ALK protein, epithelial membrane antigen, CD2, CD3, granzyme B and TIA-1 was carried out.
  • The differences between ALK-positive and ALK-negative cases were statistically analyzed.
  • RESULTS: There were 48 cases of ALK-positive ALCL and 18 cases of ALK-negative ALCL.
  • The patients with ALK-positive ALCL were younger than those with ALK-negative ALCL (P < 0.05), with the median age being 18 years and 36 years, respectively.
  • Fever, especially hyperpyrexia, was more commonly observed in ALK-positive ALCL patients than in ALK-negative ALCL patients (33 cases versus 4 cases, P < 0.05).
  • The overall survival rate and median duration of survival in patients with ALK-positive ALCL were higher and longer than those in patients with ALK-negative ALCL (80% versus 71%; 21 months versus 12.5 months, P > 0.05).
  • There were however no significant differences in histology between ALK-positive ALCL and ALK-negative ALCL.
  • "Hallmark" cells were seen in most of the ALCL cases.
  • Most ALK-positive cases belonged to the common variant (35 cases).
  • Small cell variant and sarcomatoid subtype were found only in few cases (3 cases and 2 cases, respectively).On the other hand, common variant (17 cases) constituted the majority of ALK-negative ALCL.
  • Immunohistochemical study showed that ALK-positive ALCL always expressed CD30 and epithelial membrane antigen.
  • ALK-positive ALCL more often expressed epithelial membrane antigen (100% versus 72%; P < 0.05) but less so for T-cell markers (including CD2, CD3, CD43 and CD45RO).
  • Cytotoxic molecules were more commonly expressed in ALK-positive ALCL (P > 0.05).
  • FISH showed that in ALK-positive ALCL, 1 case had normal ALK gene, 1 had deletion and multicopy and 2 had deletion.
  • On the other hand, 1 case of ALK-negative ALCL had normal ALK gene.
  • CONCLUSIONS: While there are no significant morphologic differences between ALK-positive ALCL and ALK-negative ALCL, the clinical features, immunophenotypes and genetic features of both groups vary.
  • These differences are helpful in guiding the differential diagnosis.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / metabolism. Lymphoma, Large-Cell, Anaplastic / pathology. Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] Adolescent. Adult. Age Factors. Antigens, CD30 / metabolism. Child. Child, Preschool. Diagnosis, Differential. Female. Follow-Up Studies. Gene Deletion. Humans. Male. Malignant Hyperthermia / etiology. Middle Aged. Mucin-1 / metabolism. Neoplasm Recurrence, Local. Receptor Protein-Tyrosine Kinases. Survival Rate. Young Adult

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  • (PMID = 20654121.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] Comparative Study; English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Mucin-1; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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10. Weinberg OK, Seo K, Arber DA: Prevalence of bone marrow involvement in systemic anaplastic large cell lymphoma: are immunohistochemical studies necessary? Hum Pathol; 2008 Sep;39(9):1331-40
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prevalence of bone marrow involvement in systemic anaplastic large cell lymphoma: are immunohistochemical studies necessary?
  • The frequency of bone marrow involvement in anaplastic large cell lymphoma has been reported with great variation.
  • A prior study found that anaplastic large cell lymphoma involvement of bone marrow was often not evident on routine stains and advocated using immunohistochemical studies.
  • We evaluated 70 bone marrow biopsies from 41 patients with anaplastic large cell lymphoma and found 10 morphologically involved cases (14% of all biopsies, 22% of all patients).
  • In most cases (9/10 biopsies), the involvement of the bone marrow by anaplastic large cell lymphoma was massive and, thus, was evident on the hematoxylin and eosin section.
  • To determine if the hematoxylin and eosin evaluation missed bone marrow involvement, we used a panel of antibodies including CD30, ALK-1, epithelial membrane antigen, and granzyme.
  • Only the 10 morphologically involved cases showed anaplastic large cell lymphoma cells with distinct CD30 expression.
  • Other stains highlighted only a subset of the CD30-positive cases.
  • Overall, marrow involvement in anaplastic large cell lymphoma was relatively uncommon, and when present, it was identified on hematoxylin and eosin sections.
  • [MeSH-major] Bone Marrow / pathology. Lymphoma, Large-Cell, Anaplastic / pathology
  • [MeSH-minor] Adult. Aged, 80 and over. Antigens, CD30 / immunology. Child. Child, Preschool. Clone Cells / pathology. Eosine Yellowish-(YS). Female. Hematoxylin. Humans. Immunohistochemistry. Male. Middle Aged. Protein-Tyrosine Kinases / analysis. Receptor Protein-Tyrosine Kinases. Survival Analysis

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  • (PMID = 18602674.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD30; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; TDQ283MPCW / Eosine Yellowish-(YS); YKM8PY2Z55 / Hematoxylin
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11. Hernandez C, Puangsuvan SN, Peterson A, Robinson JK: Localized perineal cutaneous nodules: a case of recurrent systemic anaplastic large-cell lymphoma. Clin Exp Dermatol; 2009 Dec;34(8):e722-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Localized perineal cutaneous nodules: a case of recurrent systemic anaplastic large-cell lymphoma.
  • We report an unusual case of localized cutaneous nodules heralding the recurrence of systemic CD30+ anaplastic large-cell lymphoma (ALCL).
  • A 47-year-old woman developed numerous violaceous nodules in the perineal and upper thigh area 3 years after multimodal treatment and complete remission of primary anaplastic large-cell CD30+ lymphoma.
  • Using immunohistochemical and T-cell gene rearrangement analysis, a recurrence of her anaplastic large-cell lymphoma was diagnosed.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / pathology. Neoplasm Recurrence, Local / pathology. Skin Neoplasms / pathology
  • [MeSH-minor] Antigens, CD30 / genetics. Cell Transformation, Neoplastic / genetics. Female. Gene Rearrangement, T-Lymphocyte / genetics. Humans. Middle Aged. Stem Cell Transplantation. Treatment Outcome

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  • (PMID = 20055841.001).
  • [ISSN] 1365-2230
  • [Journal-full-title] Clinical and experimental dermatology
  • [ISO-abbreviation] Clin. Exp. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD30
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12. Armstrong G, Szallasi A, Biegel JA, Shurtleff S, Bilaniuk LT, Womer RB, Choi JK: Early molecular detection of central nervous system relapse in a child with systemic anaplastic large cell lymphoma: case report and review of the literature. Pediatr Blood Cancer; 2005 Apr;44(4):400-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Early molecular detection of central nervous system relapse in a child with systemic anaplastic large cell lymphoma: case report and review of the literature.
  • We report a case of anaplastic large cell lymphoma (ALCL) with central nervous system relapse in an 11-year-old boy.
  • The relapse was suspected on morphologic examination of the cytospin preparations of the cerebrospinal fluid (CSF) with a WBC of 10 cells/microl.
  • The patient developed large intracranial metastases, despite systemic, and intrathecal chemotherapy.
  • This case demonstrates the feasibility of detecting ALCL in paucicellular CSF specimens and suggests that even low CSF involvement can herald massive parenchymal disease.
  • [MeSH-major] Central Nervous System Neoplasms / cerebrospinal fluid. Central Nervous System Neoplasms / pathology. Lymphoma, Large-Cell, Anaplastic / cerebrospinal fluid. Lymphoma, Large-Cell, Anaplastic / pathology

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  • (PMID = 15515044.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 25
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13. Vera L, Reategui R, Beltran B, Morales D, Capellino A, Desposorio C, Castillo J: The clinicopathological spectrum of HIV-associated lymphoma: Eleven-year-experience in a general hospital in Peru. J Clin Oncol; 2009 May 20;27(15_suppl):e19561

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The clinicopathological spectrum of HIV-associated lymphoma: Eleven-year-experience in a general hospital in Peru.
  • : e19561 Background: The clinicopathological spectrum of HIV-associated lymphomas in developing countries has not been clearly defined.
  • METHODS: This is a retrospective review of the clinical records of patients with diagnosis of HIV in our institution from March 1997 to March 2008.
  • RESULTS: Forty-eight patients with HIV-associated lymphoma were identified.
  • Forty-four cases (92%) were diagnosed with non-Hodgkin lymphoma (NHL) and 4 cases (8%) with Hodgkin lymphoma (HL).
  • From the 44 NHL cases, 40 cases (91%) were of B-cell origin; 23 cases (57.5%) had diffuse large B-cell, 9 cases (22.5%) had Burkitt, 3 cases (7.5%) had plasmablastic, 2 cases (5%) had primary CNS, 2 cases (5%) had MALT and 1 case (2.5%) had primary effusion lymphoma.
  • The remaining 4 cases (9%) were of T-cell origin; 3 cases (75%) had peripheral T-cell lymphoma NOS and 1 case (25%) was ALK-negative anaplastic large cell lymphoma.
  • Only 16 patients (33%) were receiving HAART previously the diagnosis of NHL and 33 patients (68%) received any oncology treatment.
  • Also a high proportion of T-cells lymphomas are found.

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  • (PMID = 27961062.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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14. Andorsky DJ, Yamada R, Steward K, De Vos S, Said J, Timmerman J: Expression of programmed death ligand 1 (PD-L1) by non-Hodgkin's lymphomas (NHL) and effect on tumor-associated T cells. J Clin Oncol; 2009 May 20;27(15_suppl):8526

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of programmed death ligand 1 (PD-L1) by non-Hodgkin's lymphomas (NHL) and effect on tumor-associated T cells.
  • METHODS: PD-L1 expression was analyzed in 16 NHL cell lines by flow cytometry (FC) and in 111 lymphoma specimens by immunohistochemistry (IHC) (n=92) or FC (n=19).
  • In functional studies, irradiated anaplastic large cell lymphoma (ALCL) cells were co-cultured with allogeneic T cells in the presence of anti-PD-L1 blocking antibody, and IFNγ secretion and thymidine incorporation was used to assess T cell function and proliferation.
  • To further test tumor-T cell interactions, malignant ascites from a patient with ALK+ ALCL and peripheral blood mononuclear cells from a patient with leukemic mantle cell lymphoma, both containing PD-L1-expressing tumor cells and tumor-associated T cells, were stimulated with phytohemagglutinin (a polyclonal T cell activator) and incubated with anti-PD-L1 antibody.
  • Levels of 16 inflammatory cytokines were measured as an assessment of T cell activity.
  • RESULTS: All 9 B cell lymphoma lines were negative for PD-L1, while all 5 ALCL cell lines were strongly positive.
  • One T-cell ALL line was positive, and one peripheral T cell lymphoma was negative.
  • Strong PD-L1 staining was detected by IHC in all 14 ALCL specimens and in 83% of diffuse large B cell lymphomas (DLBCL) analyzed (n=35).
  • Activity of allogeneic T cells co-cultured with irradiated ALCL cells, as measured by IFNγ secretion and proliferation, was markedly enhanced in the presence of anti-PD-L1 blocking antibody.
  • In the autologous setting using cultures of ALCL and mantle cell lymphoma specimens containing host T cells, secretion of inflammatory cytokines by tumor-associated T cells, including GMCSF, IFNγ, IL-1, IL-6, IL-8, TNFα, and MIP1α, were increased by incubation with anti-PD-L1 antibody.
  • CONCLUSIONS: PD-L1 is highly expressed in ALCL and in a majority of DLBCL.
  • PD-L1 may play a role in thwarting an effective anti-tumor immune response and represents an attractive target for lymphoma immunotherapy.

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  • (PMID = 27960901.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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15. Castillo J, Milani C, Pantanowitz L: HIV-associated anaplastic large cell lymphoma. J Clin Oncol; 2009 May 20;27(15_suppl):e19563

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] HIV-associated anaplastic large cell lymphoma.
  • : e19563 Background: Anaplastic large cell lymphoma (ALCL) is a CD30+ T-cell lymphoma that is generally unrelated to EBV in the non-HIV setting.
  • Based upon anaplastic lymphoma kinase (ALK) expression, the new WHO classification provisionally distinguishes between ALK+ (favorable) and ALK- (unfavorable) ALCL.
  • The characteristics of ALCL, such as ALK expression and EBV coinfection, in individuals with HIV infection have not been adequately evaluated.
  • The aim of this study was to investigate these features in HIV-associated ALCL cases.
  • METHODS: A MEDLINE search for all cases of HIV-associated non-cutaneous ALCL was undertaken.
  • Data regarding patient age, gender, HIV status (CD4 count, viral load, opportunistic infections), HAART, lymphoma features (B symptoms, stage, sites of involvement, immunophenotype, ALK expression, molecular studies), EBV coinfection, therapy and outcome (survival, cause of death) were extracted and analyzed.
  • ALCL was extranodal in 22 cases (96%) affecting most commonly lung, soft tissue and liver.
  • Many (78%) patients had stage IV disease and B symptoms were reported in 9 cases (50%).
  • T-cell receptor gene rearrangement was present in all cases, CD30 was positive in 22 (96%), and the vast majority (90%) were ALK-negative.
  • Therapy for ALCL was documented in 15 (67%) cases; 64% received CHOP.
  • Death was caused by either lymphoma progression (42%) or infection (58%).
  • CONCLUSIONS: HIV-associated non-cutaneous ALCL appears to affect younger individuals and is associated with EBV infection in a subset of cases.
  • Apart from marked immunosuppression, the poor prognosis of HIV-associated ALCL appears to be related to the absence of ALK expression, advanced stage at presentation with prominent extranodal disease, inadequate therapy including HAART, and poor response to CHOP.
  • Further research is needed to better understand and treat this unique HIV-associated lymphoma.

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  • (PMID = 27961064.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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16. Goldman S, Coiffier B, Reiter A, Younes A, Cairo MS, International TLS Expert Panel: A medical decision tree for the prophylaxis (P) and treatment (T) of tumor lysis syndrome (TLS): An international TLS consensus panel. J Clin Oncol; 2009 May 20;27(15_suppl):e17575

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Additionally, we recently reported an evidence based review of guidelines for the P and T of TLS (Coiffier et al, J Clin Oncol. 2008).
  • METHODS: We convened an international panel (N = 17) of experts in pediatric and adult hematological malignancies and solid tumors (ST) to develop a medical decision tree for the P and T of TLS based on the risk classification (low, medium, high) and management recommendations of Coiffier et al (J Clin Oncol.
  • 2008) Results: Patients without evidence of LTLS were assigned to either low-risk disease (LRD), medium-risk (MRD), or high-risk (HRD).
  • Risk factors included pathological classification stage, bulk, disease burden (WBC/LDH) and renal impairment/involvement.
  • MRD consisted of ALL ≤100K/mm<sup>3</sup>, AML 25-100K/mm<sup>3</sup>, BL/LL stage I/II and low LDH, childhood ALCL, DLBCL/PTCL/MCL/ATL non-bulky but elevated LDH, CLL treated with targeted therapy, and LRD with renal impairment/involvement.
  • CONCLUSIONS: This medical decision tree will facilitate the practice of management of the P and T of TLS and hopefully improve the quality of care in a cost effective manner.

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  • (PMID = 27963935.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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17. Kwak EL, Camidge DR, Clark J, Shapiro GI, Maki RG, Ratain MJ, Solomon B, Bang Y, Ou S, Salgia R: Clinical activity observed in a phase I dose escalation trial of an oral c-met and ALK inhibitor, PF-02341066. J Clin Oncol; 2009 May 20;27(15_suppl):3509

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Tumor types included colorectal, pancreatic, sarcoma, ALCL and NSCLC.

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  • (PMID = 27961297.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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18. Blum KA, Smith M, Fung H, Zalevsky J, Combs D, Ramies DA, Younes A: Phase I study of an anti-CD30 Fc engineered humanized monoclonal antibody in Hodgkin lymphoma (HL) or anaplastic large cell lymphoma (ALCL) patients: Safety, pharmacokinetics (PK), immunogenicity, and efficacy. J Clin Oncol; 2009 May 20;27(15_suppl):8531

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I study of an anti-CD30 Fc engineered humanized monoclonal antibody in Hodgkin lymphoma (HL) or anaplastic large cell lymphoma (ALCL) patients: Safety, pharmacokinetics (PK), immunogenicity, and efficacy.
  • : 8531 Background: XmAb2513 is a novel 2<sup>nd</sup>-generation humanized monoclonal antibody (mAb) directed against CD30 (a cell surface antigen expressed on Reed-Sternberg cells of HL and ALCL), with an Fc region engineered to have increased binding affinity to Fcγ receptors (FcγRs) leading to improved FcγR-dependent effector cell functions.
  • In vitro, XmAb2513 was more potent and more efficacious than 1<sup>st</sup>-generation anti-CD30 mAbs (e.g., SGN-30 & MDX-060).
  • A Phase 1 study has been initiated to examine the safety and efficacy of XmAb2513 in patients (pts) with relapsed HL and ALCL.
  • Pts receive up to 4 cycles (8 infusions) with sample collections at regular intervals for safety, PK, soluble CD30 (sCD30) and detection of immunogenicity [i.e., human Abs to humanized Abs (HAHA)].

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  • (PMID = 27960926.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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19. Oki M, Isozaki M, Nakamura N, Kikuchi A, Tsuchiya T, Arbogast P, Ogawa Y, Ando K: A multivariate analysis for the survival of nodal peripheral T-cell lymphoma (PTCL). J Clin Oncol; 2009 May 20;27(15_suppl):e19521

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A multivariate analysis for the survival of nodal peripheral T-cell lymphoma (PTCL).
  • : e19521 Background: Nodal peripheral T-cell lymphoma (PTCL) is uncommon lymphoma with various subtypes and poor prognosis.
  • However, the superiority of high-dose chemotherapy followed by autologous stem cell transplantation (ASCT) has remained inconclusive.
  • The infrequency of PTCL is an obstacle to perform a large prospective study.
  • We conducted a retrospective study of fifty six patients with three major nodal PTCL, histologically classified as PTCL-not specified (NOS, n=29), angioimmunoblastic T-cell lymphoma (AITL, n=19), and ALK-negative anaplastic large cell lymphoma (ALCL, n=8) who underwent ASCT (n=14) or not (n=42) after CT in Tokai University Hospital, Ebina General Hospital, and Hadano Red Cross Hospital, Kanagawa, Japan between 1997 and 2008.

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  • (PMID = 27960935.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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20. Lansigan F, Cooper D, Seropian S, Foss F: Autologous and allogeneic transplantation for aggressive T-cell lymphomas: A single institution experience. J Clin Oncol; 2009 May 20;27(15_suppl):8558

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Autologous and allogeneic transplantation for aggressive T-cell lymphomas: A single institution experience.
  • : 8558 Aggressive T-cell lymphomas (ATCL) represent 10-15% of non-Hodgkin lymphoma and have a worse prognosis than aggressive B-cell lymphomas.
  • Both autologous (Auto) and allogeneic (Allo) stem cell transplantation have been used as consolidation in first remission and at relapse, but the role of transplantation has not been clearly defined.
  • The Allo group consisted of 4 PTCLu, 3 angioimmunoblastic(AITL), 2 panniculitis-like, 2 cutaneous(CTCL) with large cell transformation, 2 NK-cell, 2 anaplastic large cell(ALCL), 1 hepatosplenic, 1 enteropathic, and 1 refractory CTCL.
  • The Auto group consisted of 6 PTCLu, 12 ALCL (5 Alk+, 5 Alk-, 2 Alk unk), 4 AITL, 1 CTCL with transformation, and 1 T-lymphoblastic lymphoma.
  • Median time from diagnosis to Allo or Auto was 18 and 8mo, respectively.
  • For patients with resistant or relapsed disease, Allo should be strongly considered rather than Auto.

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  • (PMID = 27960993.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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21. Schmitz N, Ziepert M, Nickelsen M, Wolf SP, Truemper L, Loeffler M, Ho A, Metzner B, Rosenwald A, Pfreundschuh M: Mature T-/NK-cell lymphomas: Prognostic factors and treatment outcome of patients treated on studies of the German High-Grade Lymphoma Study Group (DSHNHL). J Clin Oncol; 2009 May 20;27(15_suppl):8564

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mature T-/NK-cell lymphomas: Prognostic factors and treatment outcome of patients treated on studies of the German High-Grade Lymphoma Study Group (DSHNHL).
  • : 8564 Background: T-cell lymphomas represent a heterogeneous group of malignancies difficult to diagnose and to treat.
  • METHODS: Between 1993 and 2006 we treated 329 pts with ALK-positive ALCL (73 pts), ALK-negative ALCL (108 pts), PTCL, NOS (68 pts), AITL (28 pts), NK-/T-cell lymphoma (18 pts), and rare T-cell lymphomas on prospective studies.
  • RESULTS: The majority of pts with ALK-positive ALCL presented with IPI 0, 1 (62%) or IPI 2 (26%) and had an excellent overall survival (OS) of 89 % and event-free survival (EFS) of 75% at 3 yrs.
  • OS, EFS were significantly better for ALK-positive ALCL but did not significantly differ for pts in other histological subgroups.
  • In younger pts (ALK-positive ALCL were excluded) and good-risk disease (LDH <= N) there was a trend for better EFS after the addition of E to CHOP (EFS 63% vs. 48%, p = 0.065).
  • The MegaCHOEP protocol (Schmitz et al., CANCER 2006) failed to improve treatment results for younger pts with poor-risk disease (EFS at 3 yrs: 25.9%, 95% CI: 10.4-41.4); the prospective study comparing MegaCHOEP with CHOEP-14 was stopped for pts with T-cell lymphoma.
  • CONCLUSIONS: CHO(E)P results in excellent OS of pts with ALK-positive ALCL and selected pts with other histologies and low IPI.

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  • (PMID = 27961019.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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22. Bartlett N, Forero-Torres A, Rosenblatt J, Fanale M, Horning SJ, Thompson S, Sievers EL, Kennedy DA: Complete remissions with weekly dosing of SGN-35, a novel antibody-drug conjugate (ADC) targeting CD30, in a phase I dose-escalation study in patients with relapsed or refractory Hodgkin lymphoma (HL) or systemic anaplastic large cell lymphoma (sALCL). J Clin Oncol; 2009 May 20;27(15_suppl):8500

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Complete remissions with weekly dosing of SGN-35, a novel antibody-drug conjugate (ADC) targeting CD30, in a phase I dose-escalation study in patients with relapsed or refractory Hodgkin lymphoma (HL) or systemic anaplastic large cell lymphoma (sALCL).
  • : 8500 Background: A defining feature of HL and sALCL is CD30 expression on malignant cells.
  • The ADC SGN-35 comprises an anti-CD30 antibody conjugated to the antitubulin agent monomethyl auristatin E (MMAE).
  • SGN-35 causes cell cycle arrest and apoptosis by binding to CD30 on the tumor cell surface, internalizing, and releasing MMAE into the cell.
  • Pts with stable disease or better (Cheson 2007) after two 28-day cycles (6 doses) were eligible to continue SGN-35 treatment.

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  • (PMID = 27960851.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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23. Lowe EJ, Sposto R, Perkins SL, Gross TG, Finlay J, Zwick D, Abromowitch M, Children's Cancer Group Study 5941: Intensive chemotherapy for systemic anaplastic large cell lymphoma in children and adolescents: final results of Children's Cancer Group Study 5941. Pediatr Blood Cancer; 2009 Mar;52(3):335-9
ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Intensive chemotherapy for systemic anaplastic large cell lymphoma in children and adolescents: final results of Children's Cancer Group Study 5941.
  • BACKGROUND: Anaplastic large cell lymphoma (ALCL) is characterized by advanced disease at presentation (70-80% of pediatric cases) and accounts for 10-15% of all childhood lymphomas.
  • Treatment strategies for pediatric ALCL vary from short pulse B-NHL chemotherapy to prolonged leukemia like therapy.
  • METHODS: CCG-5941 used a compressed aggressive multiagent T-cell lineage chemotherapy regimen consisting of a 3-week induction therapy (vincristine, prednisone, cyclophosphamide, daunomycin, asparaginase) followed by a 3-week consolidation period (vincristine, prednisone, etoposide, 6-thioguanine, cytarabine, asparaginase, methotrexate) followed by six courses of maintenance chemotherapy at 7-week intervals (cyclophosphamide, 6-thioguanine, vincristine, prednisone, doxorubicin, asparaginase, methotrexate etoposide, cytarabine).
  • RESULTS: Eighty-six children (male 56%, female 44%) with non-localized ALCL (CD30+) were treated.
  • The majority of tumors were positive for ALK (90%) and of T lineage (83%).
  • Extranodal disease was common (mediastinum 35%, skin 15%, lung 14%, bone 12%, bone marrow 13%, liver 6%, and other viscera 17%).
  • Relapse occurred early with 17 (81%) relapses occurring within 2 years of diagnosis and 12 (57%) while receiving therapy.

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  • (PMID = 18985718.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U10 CA098543; None / None / / U10 CA098543-06; United States / NCI NIH HHS / CA / U10 CA098543-06
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS123401; NLM/ PMC2769495
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24. Forero-Torres A, Leonard JP, Younes A, Rosenblatt JD, Brice P, Bartlett NL, Bosly A, Pinter-Brown L, Kennedy D, Sievers EL, Gopal AK: A Phase II study of SGN-30 (anti-CD30 mAb) in Hodgkin lymphoma or systemic anaplastic large cell lymphoma. Br J Haematol; 2009 Jul;146(2):171-9
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  • [Title] A Phase II study of SGN-30 (anti-CD30 mAb) in Hodgkin lymphoma or systemic anaplastic large cell lymphoma.
  • SGN-30, a chimeric anti-CD30 monoclonal antibody, has demonstrated potent preclinical antitumour activity in both Hodgkin lymphoma (HL) and anaplastic large cell lymphoma (ALCL).
  • We conducted an open-label, Phase II study to determine the safety and objective response rate of SGN-30 in 79 patients with refractory/recurrent HL (n = 38) or systemic ALCL (n = 41).
  • Patients had received a median of 3 (range 1-5) prior regimens of chemotherapy or systemic therapy.
  • In the ALCL group, two patients achieved a complete response and five additional patients achieved a partial response, with response durations ranging from 27 to 1460+ d.
  • No objective responses were observed in the HL group; however, 11 patients (29%) had stable disease (duration 62-242 days).
  • Although adverse events were common, most were mild or moderate, and no specific pattern of adverse events was observed in either disease group.
  • These results demonstrate that weekly administration of SGN-30 is safe, with modest clinical activity in patients with ALCL.
  • [MeSH-major] Antibodies, Monoclonal / administration & dosage. Antineoplastic Agents / administration & dosage. Hodgkin Disease / therapy. Lymphoma, Large-Cell, Anaplastic / drug therapy


25. Goteri G, Simonetti O, Rupoli S, Piccinini G, Rubini C, Stramazzotti D, Fazioli F, Capomagi C, Leoni P, Offidani AM, Lo Muzio L: Differences in survivin location and Bcl-2 expression in CD30+ lymphoproliferative disorders of the skin compared with systemic anaplastic large cell lymphomas: an immunohistochemical study. Br J Dermatol; 2007 Jul;157(1):41-8
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  • [Title] Differences in survivin location and Bcl-2 expression in CD30+ lymphoproliferative disorders of the skin compared with systemic anaplastic large cell lymphomas: an immunohistochemical study.
  • BACKGROUND: Cutaneous CD30+ lymphoproliferative disorders (LPDs) are a spectrum of disease associated with a favourable prognosis.
  • Systemic anaplastic large cell lymphoma (ALCL), although morphologically and phenotypically similar, differs in clinical presentation and has a less favourable biological behaviour.
  • Dysregulation of apoptosis, the process regulating cell population by programmed death, can explain the differences among these disorders.
  • OBJECTIVES: We investigated the expression of two inhibitors of apoptosis, survivin and Bcl-2 protein, in serial skin lesion samples from CD30+ LPDs compared with systemic ALCL.
  • METHODS: Immunohistochemical analysis with antibodies against anaplastic lymphoma kinase (ALK)-1 protein, survivin and Bcl-2 protein was performed in 10 cutaneous CD30+ LPDs (five lymphomatoid papulosis, five ALCL) and 18 systemic ALCLs.
  • RESULTS: Cutaneous CD30+ LPDs shared a heterogeneous expression of cytoplasmic survivin with all systemic ALCLs, and of Bcl-2 with systemic ALK- ALCLs; however, they differ from systemic ALK- ALCLs because they lack nuclear survivin (P = 0.045), and from systemic ALK+ ALCLs by a higher expression of Bcl-2 (P = 0.045) and a lack of ALK-1.
  • Overall, coexpression of Bcl-2 and nuclear survivin in CD30+ LPDs was associated with a less favourable disease survival.
  • CONCLUSIONS: The different patterns of expression of Bcl-2 and survivin in CD30+ LPDs might have an impact on their different biological and clinical behaviour.
  • Moreover, nuclear localization of survivin, similarly to ALK, may be a useful marker for predicting a systemic form of ALCL with cutaneous presentation.
  • [MeSH-major] Antigens, CD30 / metabolism. Lymphoproliferative Disorders / diagnosis. Microtubule-Associated Proteins / metabolism. Neoplasm Proteins / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. Skin Neoplasms / diagnosis
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cysteine Proteinase Inhibitors / pharmacology. Diagnosis, Differential. Female. Humans. Immunohistochemistry / methods. Inhibitor of Apoptosis Proteins. Lymphoma, Large B-Cell, Diffuse / diagnosis. Male. Middle Aged. Protein-Tyrosine Kinases / metabolism. Receptor Protein-Tyrosine Kinases. Skin

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  • [ErratumIn] Br J Dermatol. 2007 Aug;157(2):431. Lomuzio, L [corrected to Lo Muzio, L]
  • (PMID = 17484779.001).
  • [ISSN] 0007-0963
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / BIRC5 protein, human; 0 / Cysteine Proteinase Inhibitors; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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26. Gualco G, Weiss LM, Bacchi CE: Expression of p63 in anaplastic large cell lymphoma but not in classical Hodgkin's lymphoma. Hum Pathol; 2008 Oct;39(10):1505-10
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of p63 in anaplastic large cell lymphoma but not in classical Hodgkin's lymphoma.
  • Immunohistochemical determination of p63 protein is frequently used in the pathologic diagnosis of nonhematological solid tumors.
  • In malignant hematological disease, p63 expression has been reported in 22% of follicular lymphoma, about 35% of diffuse large B-cell lymphoma, 23% of chronic lymphocytic leukemia, and in some cases of blast crisis of chronic myelogenous leukemia.
  • Anaplastic large cell lymphoma is a rare disease that accounts for less than 5% of all cases of non-Hodgkin's lymphoma.
  • There is little information concerning p63 expression in this specific type of lymphoma.
  • In some cases, the morphological and phenotypic features between anaplastic large cell lymphoma and classical Hodgkin's lymphoma are similar, making this differential diagnosis challenging.
  • We studied p63 expression using a tissue microarray approach in 154 cases of anaplastic large cell lymphoma, including 38% anaplastic large cell kinase positive and 62% anaplastic large cell kinase negative, and 58 Hodgkin's lymphoma cases.
  • Sixty-eight cases of anaplastic large cell lymphoma (44%) showed p63 nuclear positivity (41% of anaplastic large cell kinase positive and 47% of anaplastic large cell kinase negative).
  • Of 130 cases of systemic-anaplastic large cell lymphoma, 42% showed p63 positivity.
  • The neoplastic cells expressed p63 in 38% of the cases of CD45-negative/anaplastic large cell kinase-negative null cell-type anaplastic large cell lymphoma, a subgroup that offers the most difficulties in the differential diagnosis with classical Hodgkin's lymphoma.
  • In contrast, none of the cases of classical Hodgkin's lymphoma demonstrated any p63 expression.
  • These results demonstrate that p63 protein expression is frequently expressed in a subset of anaplastic large cell lymphoma cases and may be used as a potential tool in the differential diagnosis between anaplastic large cell lymphoma and classical Hodgkin's lymphoma.

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  • (PMID = 18620733.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA112217-03; United States / NCI NIH HHS / CA / R01 CA112217; United States / NCI NIH HHS / CA / 5R01CA082274; United States / NCI NIH HHS / CA / R01 CA112217-03; United States / NCI NIH HHS / CA / R01 CA082274-08; United States / NCI NIH HHS / CA / CA082274-08; United States / NCI NIH HHS / CA / R01 CA082274; United States / NCI NIH HHS / CA / U01 CA121947-016821; United States / NCI NIH HHS / CA / 5R01CA112217; United States / NCI NIH HHS / CA / CA121947-016821
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CKAP4 protein, human; 0 / Membrane Proteins; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Other-IDs] NLM/ NIHMS127050; NLM/ PMC2744879
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27. Huang W, Li X, Yao X, Lu Y, Li B, Sheng W, Lu H, Jin A, Zhou X: Expression of ALK protein, mRNA and fusion transcripts in anaplastic large cell lymphoma. Exp Mol Pathol; 2009 Apr;86(2):121-6
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  • [Title] Expression of ALK protein, mRNA and fusion transcripts in anaplastic large cell lymphoma.
  • Systemic anaplastic large cell lymphoma (ALCL) can be divided into two subgroups, anaplastic lymphoma kinase (ALK)-positive and ALK-negative, based on the expression of ALK protein.
  • In this study, we investigated the expression of ALK protein, mRNA and fusion transcripts involving ALK and their relationships in ALCL and analyzed formalin-fixed, paraffin-embedded tissues.
  • Our results showed that the expression of ALK protein, ALK mRNA and ALK fusion transcripts were significantly related to one another (P<0.01).
  • Consistent with the expression of ALK protein, patients presenting with ALK mRNA or ALK involved fusion transcripts were significantly younger than those lacking ALK gene alteration (P<0.01).
  • Combined detection of ALK protein, ALK mRNA and ALK fusion transcripts can complement each other to aid in the diagnosis of ALCL.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Lymphoma, Large-Cell, Anaplastic / enzymology. Lymphoma, Large-Cell, Anaplastic / genetics. Oncogene Proteins, Fusion / genetics. Protein-Tyrosine Kinases / genetics

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  • (PMID = 19135051.001).
  • [ISSN] 1096-0945
  • [Journal-full-title] Experimental and molecular pathology
  • [ISO-abbreviation] Exp. Mol. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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28. Summers TA, Moncur JT: The small cell variant of anaplastic large cell lymphoma. Arch Pathol Lab Med; 2010 Nov;134(11):1706-10
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  • [Title] The small cell variant of anaplastic large cell lymphoma.
  • Anaplastic large cell lymphomas constitute a heterogeneous group of hematopoietic neoplasms that are characterized by immunopositivity for CD30 and the presence, in varying degrees, of large, pleomorphic "hallmark" cells.
  • Primary systemic anaplastic lymphoma kinase-positive anaplastic large cell lymphomas are a subset of this group.
  • Numerous heterogeneous histomorphologic patterns have been described in anaplastic lymphoma kinase-positive anaplastic large cell lymphomas, and all patterns tend to have a better prognosis than that found in anaplastic lymphoma kinase-negative cases.
  • We provide a short review of the small cell variant of anaplastic large cell lymphoma to facilitate the diagnosis of this difficult-to-recognize entity, which may be confused with reactive processes, commonly presents with disseminated disease, and pursues an aggressive clinical course.
  • [MeSH-major] Lymphocytes / pathology. Lymphoma, Large-Cell, Anaplastic / pathology
  • [MeSH-minor] Antigens, CD30 / metabolism. Diagnosis, Differential. Humans

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  • (PMID = 21043827.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD30
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29. Colomba A, Courilleau D, Ramel D, Billadeau DD, Espinos E, Delsol G, Payrastre B, Gaits-Iacovoni F: Activation of Rac1 and the exchange factor Vav3 are involved in NPM-ALK signaling in anaplastic large cell lymphomas. Oncogene; 2008 Apr 24;27(19):2728-36
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  • [Title] Activation of Rac1 and the exchange factor Vav3 are involved in NPM-ALK signaling in anaplastic large cell lymphomas.
  • The majority of anaplastic large cell lymphomas (ALCLs) express the nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) fusion protein, which is oncogenic due to its constitutive tyrosine kinase activity.
  • Transformation by NPM-ALK not only increases proliferation, but also modifies cell shape and motility in both lymphoid and fibroblastic cells.
  • We report that the Rac1 GTPase, a known cytoskeletal regulator, is activated by NPM-ALK in ALCL cell lines (Karpas 299 and Cost) and transfected cells (lymphoid Ba/F3 cells, NIH-3T3 fibroblasts).
  • Moreover, Vav3 is phosphorylated in NPM-ALK positive biopsies from patients suffering from ALCL, demonstrating the pathological relevance of this observation.
  • [MeSH-major] Guanine Nucleotide Exchange Factors / metabolism. Lymphoma, Large-Cell, Anaplastic / enzymology. Protein-Tyrosine Kinases / metabolism. Protein-Tyrosine Kinases / physiology. Proto-Oncogene Proteins c-vav / metabolism. Signal Transduction / physiology. rac1 GTP-Binding Protein / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Humans. Mice. NIH 3T3 Cells. Nuclear Proteins / physiology. Phosphatidylinositol 3-Kinases / physiology. Receptor Protein-Tyrosine Kinases. src-Family Kinases / physiology

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  • (PMID = 17998938.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Guanine Nucleotide Exchange Factors; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins c-vav; 0 / VAV3 protein, human; 0 / Vav3 protein, mouse; 117896-08-9 / nucleophosmin; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 2.7.10.2 / CSK tyrosine-protein kinase; EC 2.7.10.2 / src-Family Kinases; EC 3.6.5.2 / rac1 GTP-Binding Protein
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30. Passoni L, Gallo B, Biganzoli E, Stefanoni R, Massimino M, Di Nicola M, Gianni AM, Gambacorti-Passerini C: In vivo T-cell immune response against anaplastic lymphoma kinase in patients with anaplastic large cell lymphomas. Haematologica; 2006 Jan;91(1):48-55
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  • [Title] In vivo T-cell immune response against anaplastic lymphoma kinase in patients with anaplastic large cell lymphomas.
  • BACKGROUND AND OBJECTIVES: Anaplastic lymphoma kinase (ALK) oncogenic fusion proteins, expressed in about 60% of anaplastic large cell lymphomas (ALCL), are tumor-specific molecular targets for such a malignancy.
  • DESIGN AND METHODS: The frequency and the functional phenotype of the anti-ALK CD8 precursor repertoire in freshly isolated peripheral blood mononuclear cells (PBMC) from healthy donors and ALK-positive patients were determined by major histocompatibility complex (MHC)/tetrameric analyses.
  • In addition, the ability of the anti-ALK immune response to specifically lyse ALK-positive lymphoma cells was investigated by in vitro stimulation with ALK-derived peptide p280-89.
  • RESULTS: Tetrameric MHC/peptide complexes revealed high frequencies of CD8/ALK-tetramer-positive cells both in patients and in healthy individuals.
  • However, the functional phenotype of the CD8/ALK-tetramer-positive lymphocytes showed the presence of effector and memory T lymphocytes only in patients.
  • A polyclonal ALK-specific tumor-reactive T-cell line was isolated from patients' peripheral blood lymphocytes.
  • INTERPRETATION AND CONCLUSIONS: The presence of an anti-ALK effector/memory lymphocyte population in the peripheral blood of ALK-positive patients indicates an in vivo antigenic challenge.
  • Thus, ALK is a lymphoma-associated antigen suitable for immune interventions.
  • The high number of anti-ALK memory CD8 T cells present in patients' PBMC may represent a valid source of activated CTL suitable for cancer cell lysis.
  • [MeSH-major] CD8-Positive T-Lymphocytes / immunology. Lymphoma, Large-Cell, Anaplastic / immunology. Protein-Tyrosine Kinases / immunology

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  • (PMID = 16434370.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Cancer Vaccines; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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31. Ries S, Rnjak L, Mitrović Z, Kuvezdić KG, Nola M, Sucić M: CD13+ anaplastic large cell lymphoma with leukemic presentation and additional chromosomal abnormality. Diagn Cytopathol; 2010 Feb;38(2):141-6
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  • [Title] CD13+ anaplastic large cell lymphoma with leukemic presentation and additional chromosomal abnormality.
  • Anaplastic large cell lymphoma (ALCL) is a highly malignant neoplasm characterized by pleomorphic appearance, different immunophenotypes and variable sites of involvement.
  • Expression of myeloid-associated markers in anaplastic large cell lymphomas may mislead the medical team and result in delay of diagnosis due to unusual phenotype.
  • It is important to diagnose this type of tumors and distinguish it from myeloid neoplasms (extramedullary myeloid cell tumors and histiocytic tumors) since therapy and prognosis are significantly different.A 16-year-old female patient presented with fever, lymphadenopathy, and high white blood cell count.
  • Diagnosing a CD13+ ALCL with leukemic presentation with additional cytogenetic abnormality (duplication 5q35) was a significant diagnostic challenge.This combination of features, unusual for lymphoma, should be considered in differential diagnosis of myeloid neoplasms and fatal infections.
  • [MeSH-major] Antigens, CD13 / biosynthesis. Chromosome Aberrations. Lymphoma, Large-Cell, Anaplastic / pathology. Lymphoma, Large-Cell, Anaplastic / physiopathology
  • [MeSH-minor] Adolescent. Cell Separation. Fatal Outcome. Female. Flow Cytometry. Humans. Immunohistochemistry. Immunophenotyping. In Situ Hybridization, Fluorescence

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  • (PMID = 19760763.001).
  • [ISSN] 1097-0339
  • [Journal-full-title] Diagnostic cytopathology
  • [ISO-abbreviation] Diagn. Cytopathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.4.11.2 / Antigens, CD13
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32. Ardigò M, Marulli GC, Cota C, Mastroianni A, Berardesca E: Bexarotene and interferon-alpha combination therapy in a patient affected by relapsing anaplastic large cell lymphoma with cutaneous involvement. J Drugs Dermatol; 2007 Feb;6(2):216-9
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  • [Title] Bexarotene and interferon-alpha combination therapy in a patient affected by relapsing anaplastic large cell lymphoma with cutaneous involvement.
  • A 74-year-old man presented with relapsing systemic anaplastic large cell lymphoma (ALCL) with cutaneous involvement who had a third recurrence of cutaneous lesions associated with inguinal lymphonodes enlargement.
  • Two months after stopping therapy, lymphonodal relapse of the lymphoma was seen; however, cutaneous lesions were still in complete remission.
  • Association of low dose bexarotene with interferon-xalphaseems to represent a possible alternative therapy for relapsing systemic ALCL presenting as prevalent cutaneous involvement in patients with severe worsening of general conditions.
  • In our case, this protocol was unable to maintain a longer disease free survival in comparison with the 2 previous polychemotherapy cycles.
  • Further extended studies are required in order to define the possible rule of this combination therapy in relapsing systemic ALCL.
  • [MeSH-major] Interferon-alpha / therapeutic use. Lymphoma, Large B-Cell, Diffuse / drug therapy. Skin Neoplasms / drug therapy. Tetrahydronaphthalenes / therapeutic use
  • [MeSH-minor] Aged. Disease-Free Survival. Drug Therapy, Combination. Humans. Lymph Nodes / pathology. Male. Recurrence. Remission Induction / methods. Salvage Therapy / methods

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  • (PMID = 17373182.001).
  • [ISSN] 1545-9616
  • [Journal-full-title] Journal of drugs in dermatology : JDD
  • [ISO-abbreviation] J Drugs Dermatol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interferon-alpha; 0 / Tetrahydronaphthalenes; A61RXM4375 / bexarotene
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33. Anastasov N, Bonzheim I, Rudelius M, Klier M, Dau T, Angermeier D, Duyster J, Pittaluga S, Fend F, Raffeld M, Quintanilla-Martinez L: C/EBPβ expression in ALK-positive anaplastic large cell lymphomas is required for cell proliferation and is induced by the STAT3 signaling pathway. Haematologica; 2010 May;95(5):760-7
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  • [Title] C/EBPβ expression in ALK-positive anaplastic large cell lymphomas is required for cell proliferation and is induced by the STAT3 signaling pathway.
  • BACKGROUND: Anaplastic lymphoma kinase (ALK)-positive anaplastic large cell lymphoma is characterized by the t(2;5) chromosomal translocation, resulting in the expression of a fusion protein formed of nucleophosmin (NPM) and ALK.
  • Recently, we reported the abnormal expression of the transcription factor CCAAT/enhancer binding protein-beta (C/EBPbeta) in ALK-positive anaplastic large cell lymphomas, and demonstrated its dependence on NPM-ALK activity.
  • DESIGN AND METHODS: In this study, the role of C/EBPbeta in proliferation and survival of ALK-positive anaplastic large cell lymphomas was investigated, as well as the mechanism of its expression and activity.
  • RESULTS: Interference with C/EBPbeta expression resulted in a dramatic decrease in cell proliferation in ALK-positive anaplastic large cell lymphomas, with a mild induction of apoptosis after 6 days.
  • Down-regulation of STAT3 resulted in a marked decrease in C/EBPbeta mRNA and protein levels with impairment in cell proliferation and viability, underscoring the important role of these two proteins in ALK-mediated oncogenesis.
  • [MeSH-major] CCAAT-Enhancer-Binding Protein-beta / biosynthesis. Cell Proliferation. Gene Expression Regulation, Neoplastic. Lymphoma, Large-Cell, Anaplastic / enzymology. Receptor Protein-Tyrosine Kinases / biosynthesis. STAT3 Transcription Factor / physiology. Signal Transduction
  • [MeSH-minor] Animals. Cell Line. Cell Line, Transformed. Cell Line, Tumor. Cell Survival / genetics. Down-Regulation / genetics. Humans. Mice


34. Piccaluga PP, Gazzola A, Mannu C, Agostinelli C, Bacci F, Sabattini E, Sagramoso C, Piva R, Roncolato F, Inghirami G, Pileri SA: Pathobiology of anaplastic large cell lymphoma. Adv Hematol; 2010;:345053
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  • [Title] Pathobiology of anaplastic large cell lymphoma.
  • The authors revise the concept of anaplastic large cell lymphoma (ALCL) in the light of the recently updated WHO classification of Tumors of Hematopoietic and Lymphoid Tissues both on biological and clinical grounds.
  • The clinical features of ALCL are presented by underlining the difference in terms of response to therapy and survival between the ALK-positive and ALK-negative forms.

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  • (PMID = 21331150.001).
  • [ISSN] 1687-9112
  • [Journal-full-title] Advances in hematology
  • [ISO-abbreviation] Adv Hematol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC3038421
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35. Escobosa Sánchez OM, Herrero Hernández A, Acha García T: [Endobronchial anaplastic large cell lymphoma in childhood]. An Pediatr (Barc); 2009 May;70(5):449-52
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  • [Title] [Endobronchial anaplastic large cell lymphoma in childhood].
  • [Transliterated title] Linfoma anaplásico de células grandes endobronquial en la infancia.
  • Anaplastic large cell lymphoma is a very rare disease in childhood.
  • The most common location of this lymphoma is lymph node and skin, with endobronchial involvement being extremely rare.
  • We report a case of a 10-year-old boy diagnosed by chance with an endobronchial anaplastic large cell lymphoma, while he was being investigated for a a benign bone disease, due to the initial absence of respiratory symptoms.
  • [MeSH-major] Bronchial Neoplasms. Lymphoma, Large-Cell, Anaplastic

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  • (PMID = 19375996.001).
  • [ISSN] 1695-4033
  • [Journal-full-title] Anales de pediatría (Barcelona, Spain : 2003)
  • [ISO-abbreviation] An Pediatr (Barc)
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Spain
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36. Belousova IE, Kazakov DV, Sosna B, Sulc M, Michal M: [Small-cell variant of CD30+ -anaplastic large-cell lymphoma of the skin]. Arkh Patol; 2008 Mar-Apr;70(2):40-3
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  • [Title] [Small-cell variant of CD30+ -anaplastic large-cell lymphoma of the skin].
  • Three cases of the so-called variant of primary cutaneous CD30+ anaplastic large cell lymphoma (ALCL) are presented.
  • Microscopically, the tumors were composed of small cells with irregular nuclei that were immunohistochemically positive for CD3, CD5, CD7, and CD30 and negative for B-cell markers; there was focal ALK-1 positivity in 1 case.
  • Fhedium to large CD30+ cells were rarely found scattered in the infiltrate.
  • Chemotherapy was performed and finally the patient underwent allogenic bone marrow transplantation; he died 3 years after the original diagnosis due to acute graft-versus-host disease and sepsis.
  • [MeSH-major] Antigens, CD30. Lymphoma, Large B-Cell, Diffuse / pathology. Skin Neoplasms / pathology
  • [MeSH-minor] Aged. Antigens, CD / immunology. Cell Size. Gene Rearrangement, B-Lymphocyte / immunology. Gene Rearrangement, T-Lymphocyte / immunology. Humans. Immunoglobulin Heavy Chains / immunology. Male. Middle Aged. Receptors, Antigen, T-Cell / immunology


37. Vaid R, Cohen B: Primary cutaneous CD30 positive anaplastic large cell lymphoma in an adolescent. Pediatr Dermatol; 2009 Nov-Dec;26(6):721-4
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  • [Title] Primary cutaneous CD30 positive anaplastic large cell lymphoma in an adolescent.
  • We present a case of a 14-year-old boy with a large ulcerated plaque on the scalp for 6 months, who was found to have primary cutaneous CD30-positive, anaplastic kinase-negative, anaplastic large cell lymphoma with post-auricular lymphadenopathy.
  • MRI, bone marrow biopsy, and laboratory data demonstrated no other systemic involvement.
  • Very few cases of primary cutaneous CD30-positive anaplastic large cell lymphoma in the pediatric population have been reported, and our case represents one of the first pediatric patients with local lymph node involvement.
  • [MeSH-major] Antigens, CD30 / metabolism. Lymphoma, Large B-Cell, Diffuse / pathology. Scalp / metabolism. Scalp / pathology. Skin Neoplasms / pathology

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  • (PMID = 20199449.001).
  • [ISSN] 1525-1470
  • [Journal-full-title] Pediatric dermatology
  • [ISO-abbreviation] Pediatr Dermatol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Antimetabolites, Antineoplastic; YL5FZ2Y5U1 / Methotrexate
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38. Riera L, Lasorsa E, Ambrogio C, Surrenti N, Voena C, Chiarle R: Involvement of Grb2 adaptor protein in nucleophosmin-anaplastic lymphoma kinase (NPM-ALK)-mediated signaling and anaplastic large cell lymphoma growth. J Biol Chem; 2010 Aug 20;285(34):26441-50
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  • [Title] Involvement of Grb2 adaptor protein in nucleophosmin-anaplastic lymphoma kinase (NPM-ALK)-mediated signaling and anaplastic large cell lymphoma growth.
  • Most anaplastic large cell lymphomas (ALCL) express oncogenic fusion proteins derived from chromosomal translocations or inversions of the anaplastic lymphoma kinase (ALK) gene.
  • Frequently ALCL carry the t(2;5) translocation, which fuses the ALK gene to the nucleophosmin (NPM1) gene.
  • The transforming activity mediated by NPM-ALK fusion induces different pathways that control proliferation and survival of lymphoma cells.
  • Grb2 is an adaptor protein thought to play an important role in ALK-mediated transformation, but its interaction with NPM-ALK, as well as its function in regulating ALCL signaling pathways and cell growth, has never been elucidated.
  • Finally, shRNA knockdown experiments showed that Grb2 regulates primarily the NPM-ALK-mediated phosphorylation of SHP2 and plays a key role in ALCL cell growth.
  • [MeSH-major] Cell Proliferation. GRB2 Adaptor Protein / metabolism. Lymphoma, Large-Cell, Anaplastic / pathology. Oncogene Proteins, Fusion / metabolism. Protein-Tyrosine Kinases / metabolism. Signal Transduction
  • [MeSH-minor] Binding Sites. Humans. Nuclear Proteins / genetics. Nuclear Proteins / metabolism. Phosphorylation. Protein Binding. Protein Tyrosine Phosphatase, Non-Receptor Type 11. Receptor Protein-Tyrosine Kinases. Translocation, Genetic. Tumor Cells, Cultured

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  • (PMID = 20554525.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Grant] International / European Research Council / / 242965
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / GRB2 Adaptor Protein; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 117896-08-9 / nucleophosmin; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 11
  • [Other-IDs] NLM/ PMC2924075
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39. Koreen IV, Cho RI, Frueh BR, Elner VM: Primary cutaneous anaplastic large cell lymphoma of the medial canthus and orbit. Ophthal Plast Reconstr Surg; 2009 Jan-Feb;25(1):63-5
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  • [Title] Primary cutaneous anaplastic large cell lymphoma of the medial canthus and orbit.
  • Biopsy revealed CD30+ anaplastic large cell lymphoma.
  • Systemic evaluation for lymphoma was negative, and he underwent local radiotherapy.
  • The lesion regressed completely, and he has remained disease free for 7 months.
  • CD30+ anaplastic large cell lymphoma of the periocular skin and orbit are usually distinct, exceedingly rare entities; no reported cases had simultaneous involvement of both tissues.
  • The authors present the first reported case, to their knowledge, of simultaneous skin and orbital involvement by anaplastic large cell lymphoma.
  • [MeSH-major] Eyelid Neoplasms / pathology. Lymphoma, Large-Cell, Anaplastic / pathology. Orbital Neoplasms / pathology. Skin Neoplasms / pathology
  • [MeSH-minor] Antigens, CD3 / analysis. Antigens, CD30 / analysis. Humans. Immunoenzyme Techniques. Male. Middle Aged. Tomography, X-Ray Computed

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  • (PMID = 19273934.001).
  • [ISSN] 1537-2677
  • [Journal-full-title] Ophthalmic plastic and reconstructive surgery
  • [ISO-abbreviation] Ophthal Plast Reconstr Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD3; 0 / Antigens, CD30
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40. Bonvini P, Zorzi E, Mussolin L, Monaco G, Pigazzi M, Basso G, Rosolen A: The effect of the cyclin-dependent kinase inhibitor flavopiridol on anaplastic large cell lymphoma cells and relationship with NPM-ALK kinase expression and activity. Haematologica; 2009 Jul;94(7):944-55
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  • [Title] The effect of the cyclin-dependent kinase inhibitor flavopiridol on anaplastic large cell lymphoma cells and relationship with NPM-ALK kinase expression and activity.
  • BACKGROUND: The loss of cell cycle regulation due to abnormal function of cyclin-dependent kinases (cdk) occurs in tumors and leads to genetic instability of chemotherapy-resistant cells.
  • In this study, we investigated the effect of the cdk inhibitor flavopiridol in anaplastic large cell lymphomas, in which unrestrained proliferation depends on NPM-ALK tyrosine kinase activity.
  • DESIGN AND METHODS: Effects of flavopiridol were examined in ALK-positive and -negative anaplastic large cell lymphoma cells by means of immunoblotting and immunofluorescence analyses to assess cdk expression and activity, quantitative real time reverse transcriptase polymerase chain reaction to measure drug-induced changes in transcription, and FACS analyses to monitor changes in proliferation and survival.
  • RESULTS: Treatment with flavopiridol resulted in growth inhibition of anaplastic large cell lymphoma cells, along with accumulation of subG(1) cells and disappearance of S phase without cell cycle arrest.
  • This correlated with induction of cell death through rapid mitochondrial damage, inhibition of DNA synthesis, and down-regulation of anti-apoptotic proteins and transcripts.
  • Notably, flavopiridol was less active in ALK-positive cells, as apoptosis was observed at higher concentrations and later time points, and resistance to treatment was observed in cells maintaining NPM-ALK signaling.
  • NPM-ALK inhibition affected proliferation but not survival of anaplastic large cell lym-phoma cells, whereas it resulted in a dramatic increase in apoptosis when combined with flavopiridol.
  • CONCLUSIONS: This work provides the first demonstration that targeting cdk is effective against anaplastic large cell lymphoma cells, and proves the critical role of NPM-ALK in the regulation of responsiveness of tumor cells with cdk dysregulation.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Flavonoids / pharmacology. Gene Expression Regulation, Neoplastic. Lymphoma, Large-Cell, Anaplastic / drug therapy. Piperidines / pharmacology. Protein-Tyrosine Kinases / biosynthesis
  • [MeSH-minor] Apoptosis. Bromodeoxyuridine / pharmacology. Cell Cycle. Cell Separation. Cell Survival. Dose-Response Relationship, Drug. Humans. Reverse Transcriptase Polymerase Chain Reaction. Subcellular Fractions. Time Factors


41. Bakshi NA, Finn WG, Schnitzer B, Valdez R, Ross CW: Fascin expression in diffuse large B-cell lymphoma, anaplastic large cell lymphoma, and classical Hodgkin lymphoma. Arch Pathol Lab Med; 2007 May;131(5):742-7
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  • [Title] Fascin expression in diffuse large B-cell lymphoma, anaplastic large cell lymphoma, and classical Hodgkin lymphoma.
  • Fascin is a sensitive marker for classical Reed-Sternberg cells and has a high negative predictive value for diagnosis of classical Hodgkin lymphoma (CHL).
  • Fascin has been used to distinguish CHL from non-Hodgkin lymphoma.
  • Recently, it was shown that fascin might not help differentiate CHL from anaplastic large cell lymphoma (ALCL).
  • Moreover, fascin has not been extensively studied in the context of other large cell lymphomas.
  • OBJECTIVE: To analyze fascin expression in diffuse large B-cell lymphoma (DLBCL) and also reexamine its usefulness in discriminating CHL from ALCL.
  • DESIGN: Formalin-fixed, paraffin-embedded tissue samples from 41 cases of DLBCL, 30 cases of CHL, and 30 cases of ALCL were analyzed.
  • Fascin expression was compared across each type of lymphoma with additional correlation between fascin positivity and ALK-1 expression in ALCL performed.
  • RESULTS: Only 6 (14.6%) of 41 cases of DLBCL stained positively for fascin, with most neoplastic large cells exhibiting a weak staining pattern.
  • Fifteen (50%) of 30 cases of ALCL showed positivity for fascin, with most large cells staining strongly.
  • All 30 cases of CHL demonstrated intense positive staining.
  • Sixty percent of fascin-positive ALCLs were positive for ALK-1, while 66.7% of fascin-negative ALCLs were positive for ALK-1.
  • CONCLUSIONS: Fascin is highly sensitive for CHL and has a very high negative predictive value (100% in this series) for distinguishing CHL from DLBCL or ALCL.
  • However, the specificity and positive predictive value for fascin are much higher in distinguishing CHL from DLBCL than in distinguishing CHL from ALCL.
  • Expression of fascin appears more useful in the differential diagnosis of CHL versus DLBCL than in the differential diagnosis of CHL versus ALCL.
  • [MeSH-major] Biomarkers, Tumor / analysis. Carrier Proteins / biosynthesis. Hodgkin Disease / metabolism. Lymphoma, B-Cell / metabolism. Lymphoma, Large B-Cell, Diffuse / metabolism. Microfilament Proteins / biosynthesis
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Male. Middle Aged. Predictive Value of Tests. Sensitivity and Specificity


42. Kim YC, Yang WI, Lee MG, Kim SN, Cho KH, Lee SJ, Lee MW, Koh JK: Epstein-Barr virus in CD30 anaplastic large cell lymphoma involving the skin and lymphomatoid papulosis in South Korea. Int J Dermatol; 2006 Nov;45(11):1312-6
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  • [Title] Epstein-Barr virus in CD30 anaplastic large cell lymphoma involving the skin and lymphomatoid papulosis in South Korea.
  • AIM: To elucidate the possible association of EBV with CD30+ anaplastic large cell lymphoma (ALCL) involving the skin and lymphomatoid papulosis (LyP) in South Korea.
  • METHODS: In situ hybridization for EBV-encoded small RNA (EBER) and immunohistochemistry including viral latent membrane protein-1 (LMP-1) were performed on formalin-fixed, paraffin-embedded skin specimens of 26 cases of LyP and 16 cases of CD30+ ALCL involving the skin which were selected from six university hospital medical centers in South Korea.
  • RESULTS: In situ hybridization studies showed positivity of the neoplastic cells for EBER in two of 16 cases of CD30+ ALCL and in none of the cases of LyP.
  • One EBER-positive case was cutaneous CD30+ ALCL with concurrent lymph node involvement.
  • The other was CD30+ ALCL involving the skin and other organs, including lymph nodes, bone, lung, and spleen.
  • Immunostaining for LMP-1 was also positive only for the two cases of EBER-positive CD30+ ALCL.
  • CONCLUSION: LyP and primary cutaneous CD30+ ALCL are very rarely associated with EBV in South Korea.
  • [MeSH-major] Epstein-Barr Virus Infections / pathology. Herpesvirus 4, Human / growth & development. Lymphoma, Large-Cell, Anaplastic / pathology. Lymphomatoid Papulosis / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Antigens, CD20 / analysis. Antigens, CD3 / analysis. Antigens, CD30 / analysis. Female. Humans. Immunohistochemistry. In Situ Hybridization. Korea. Male. Middle Aged. RNA, Viral / genetics. Viral Matrix Proteins / analysis

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  • (PMID = 17076712.001).
  • [ISSN] 0011-9059
  • [Journal-full-title] International journal of dermatology
  • [ISO-abbreviation] Int. J. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD20; 0 / Antigens, CD3; 0 / Antigens, CD30; 0 / EBV-associated membrane antigen, Epstein-Barr virus; 0 / Epstein-Barr virus encoded RNA 1; 0 / Epstein-Barr virus encoded RNA 2; 0 / RNA, Viral; 0 / Viral Matrix Proteins
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43. Li C, Takino H, Eimoto T, Ishida T, Inagaki A, Ueda R, Suzuki R, Yoshino T, Nakagawa A, Nakamura S, Inagaki H: Prognostic significance of NPM-ALK fusion transcript overexpression in ALK-positive anaplastic large-cell lymphoma. Mod Pathol; 2007 Jun;20(6):648-55
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  • [Title] Prognostic significance of NPM-ALK fusion transcript overexpression in ALK-positive anaplastic large-cell lymphoma.
  • In anaplastic large-cell lymphomas positive for anaplastic lymphoma kinase (ALK) protein, the ALK gene is most commonly fused to the NPM gene, and less commonly to TPM3, TFG, ATIC, and other rare genes.
  • Although this lymphoma is generally associated with a favorable clinical outcome, 25% of the patients die of the disease within 5 years.
  • In 26 cases of ALK(+) anaplastic large-cell lymphoma, the RT-PCR assay showed that the ALK was fused to NPM in 21 cases, to TPM3 in three, and to TFG in one.
  • Overexpression of the NPM-ALK fusion transcript may be associated with a poor prognosis of the patients with ALK(+) anaplastic large-cell lymphomas.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / metabolism. Nuclear Proteins / biosynthesis. Oncogene Proteins, Fusion / biosynthesis. Protein-Tyrosine Kinases / biosynthesis

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  • (PMID = 17464320.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Fixatives; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 117896-08-9 / nucleophosmin; 1HG84L3525 / Formaldehyde; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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44. Boudova L, Kazakov DV, Jindra P, Sima R, Vanecek T, Kuntscher V, Vera V, Bouda J, Michal M: Primary cutaneous histiocyte and neutrophil-rich CD30+ and CD56+ anaplastic large-cell lymphoma with prominent angioinvasion and nerve involvement in the forehead and scalp of an immunocompetent woman. J Cutan Pathol; 2006 Aug;33(8):584-9
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  • [Title] Primary cutaneous histiocyte and neutrophil-rich CD30+ and CD56+ anaplastic large-cell lymphoma with prominent angioinvasion and nerve involvement in the forehead and scalp of an immunocompetent woman.
  • BACKGROUND: Cutaneous lymphomas co-expressing CD56 and CD30 are very rare.
  • They share a clinicopathological overlap with natural killer- (NK)/T-cell lymphomas and anaplastic large-cell lymphomas (ALCLs), two entities with widely disparate clinical behavior.
  • METHODS: We present a case of an immunocompetent 57-year-old Caucasian woman with a rapidly growing, angiodestructive and neuroinvasive primary cutaneous ALCL (PCALCL).
  • The neoplastic population of large anaplastic CD30+ and CD56+ T cells was masked by a massive admixture of histiocytes and neutrophils.
  • Additionally, high-dose chemotherapy with autologous peripheral blood stem-cell transplantation was administered as a consolidation of complete remission, in which she has remained for 6 years.
  • CONCLUSIONS: This is the first CD30+ and CD56+ primary skin lymphoma to be reported on the head.
  • The presented case carries a remarkable combination of clinicopathological features of PCALCL and NK-/T-cell lymphoma.
  • [MeSH-major] Antigens, CD30 / analysis. Antigens, CD56 / analysis. Lymphoma, Large B-Cell, Diffuse / pathology. Skin Neoplasms / pathology
  • [MeSH-minor] Female. Forehead. Head and Neck Neoplasms / blood supply. Head and Neck Neoplasms / drug therapy. Head and Neck Neoplasms / immunology. Head and Neck Neoplasms / pathology. Histiocytes / cytology. Humans. Middle Aged. Neutrophils / cytology. Scalp / blood supply. Scalp / drug effects. Scalp / innervation. Scalp / pathology. Stem Cell Transplantation

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  • (PMID = 16919035.001).
  • [ISSN] 0303-6987
  • [Journal-full-title] Journal of cutaneous pathology
  • [ISO-abbreviation] J. Cutan. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Antigens, CD56
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45. Leong MY, English M, McMullan D, Ramani P: Aberrant expression of beta-HCG in anaplastic large cell lymphoma. Pediatr Dev Pathol; 2008 May-Jun;11(3):230-4
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  • [Title] Aberrant expression of beta-HCG in anaplastic large cell lymphoma.
  • We report a case of anaplastic large cell lymphoma (ALCL) showing aberrant expression of beta subunit of human chorionic gonadotrophin (beta-HCG).
  • Biopsy of the mass revealed a malignant neoplasm composed of large, pleomorphic cells with prominent nucleoli.
  • These malignant cells showed positive staining with CD30, ALK, epithelial membrane antigen, and beta-HCG.
  • Chromosomal analysis showed t(2;5)(p23;q35) translocation, and polymerase chain reaction demonstrated T-cell receptor gene rearrangement.
  • The patient did not respond well to chemotherapy, and he died 8 months after the diagnosis.
  • To the best of our knowledge, this is the 1st case of ALCL showing aberrant expression of beta-HCG and associated with a raised serum level of beta-HCG.
  • [MeSH-major] Chorionic Gonadotropin, beta Subunit, Human / biosynthesis. Lymphoma, Large-Cell, Anaplastic / metabolism. Lymphoma, Large-Cell, Anaplastic / pathology
  • [MeSH-minor] Adolescent. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Clinical Trials, Phase II as Topic. Diagnosis, Differential. Fatal Outcome. Gene Rearrangement, T-Lymphocyte. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Male. Neoplasms, Germ Cell and Embryonal / pathology. Polymerase Chain Reaction. Translocation, Genetic

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  • (PMID = 17990918.001).
  • [ISSN] 1093-5266
  • [Journal-full-title] Pediatric and developmental pathology : the official journal of the Society for Pediatric Pathology and the Paediatric Pathology Society
  • [ISO-abbreviation] Pediatr. Dev. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chorionic Gonadotropin, beta Subunit, Human
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46. Chuang SS, Hsieh YC, Ye H, Hwang WS: Lymphohistiocytic anaplastic large cell lymphoma involving skin: a diagnostic challenge. Pathol Res Pract; 2009;205(4):283-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lymphohistiocytic anaplastic large cell lymphoma involving skin: a diagnostic challenge.
  • Systemic anaplastic large cell lymphoma (ALCL) involving the skin should be differentiated from primary cutaneous CD30-positive T-cell lymphoproliferative disorders.
  • The lymphohistiocytic variant of ALCL (LH-ALCL) is rich in reactive histiocytes with relatively few neoplastic cells, which pose a diagnostic challenge.
  • We present a case of LH-ALCL involving skin mimicking granulomatous inflammation.
  • Biopsy of the cervical lymph node showed LH-ALCL with null cell phenotype.
  • Microscopically, the cutaneous lesion was located predominately around the hair follicle, with numerous reactive histiocytes and scanty medium-sized lymphoma cells expressing CD30 and anaplastic lymphoma kinase (ALK) protein.
  • Furthermore, an ALK gene rearrangement was demonstrated by locus-specific interphase fluorescent in situ hybridization, confirming cutaneous involvement with LH-ALCL.
  • LH-ALCL involving the skin is a rare event, and the numerous reactive histiocytes may mask scanty tumor cells.
  • In addition to B-and T-cell markers, (dermato) pathologists must be aware of this entity in cutaneous lymphohistiocytic proliferations and perform immunostaining for CD30 and ALK to reach a correct diagnosis.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / pathology. Skin Neoplasms / pathology
  • [MeSH-minor] Adult. Antigens, CD30 / metabolism. Gene Rearrangement. Histiocytes / pathology. Humans. In Situ Hybridization, Fluorescence. Male. Protein-Tyrosine Kinases / genetics. Protein-Tyrosine Kinases / metabolism. Receptor Protein-Tyrosine Kinases

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  • (PMID = 19091487.001).
  • [ISSN] 1618-0631
  • [Journal-full-title] Pathology, research and practice
  • [ISO-abbreviation] Pathol. Res. Pract.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, CD30; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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47. Jundt F, Raetzel N, Müller C, Calkhoven CF, Kley K, Mathas S, Lietz A, Leutz A, Dörken B: A rapamycin derivative (everolimus) controls proliferation through down-regulation of truncated CCAAT enhancer binding protein {beta} and NF-{kappa}B activity in Hodgkin and anaplastic large cell lymphomas. Blood; 2005 Sep 1;106(5):1801-7
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  • [Title] A rapamycin derivative (everolimus) controls proliferation through down-regulation of truncated CCAAT enhancer binding protein {beta} and NF-{kappa}B activity in Hodgkin and anaplastic large cell lymphomas.
  • In this study, we provide evidence that RAD has profound antiproliferative activity in vitro and in NOD/SCID mice in vivo against Hodgkin lymphoma (HL) and anaplastic large cell lymphoma (ALCL) cells.
  • Moreover, we identified 2 molecular mechanisms that showed how RAD exerts antiproliferative effects in HL and ALCL cells.
  • Pharmacologic inhibition of the mTOR pathway by RAD therefore interferes with essential proliferation and survival pathways in HL and ALCL cells and might serve as a novel treatment option.
  • [MeSH-major] CCAAT-Enhancer-Binding Protein-beta / metabolism. Cell Proliferation / drug effects. Hodgkin Disease / metabolism. Lymphoma, Large B-Cell, Diffuse / metabolism. NF-kappa B / metabolism. Sirolimus / analogs & derivatives
  • [MeSH-minor] Animals. Cell Cycle / drug effects. Cell Cycle / physiology. Cell Line, Tumor. Down-Regulation / drug effects. Everolimus. Humans. Mice. Mice, Inbred NOD. Mice, SCID. Transplantation, Heterologous

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  • (PMID = 15886325.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Protein-beta; 0 / NF-kappa B; 9HW64Q8G6G / Everolimus; W36ZG6FT64 / Sirolimus
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48. Franchina M, Kadin ME, Abraham LJ: Polymorphism of the CD30 promoter microsatellite repressive element is associated with development of primary cutaneous lymphoproliferative disorders. Cancer Epidemiol Biomarkers Prev; 2005 May;14(5):1322-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Polymorphism of the CD30 promoter microsatellite repressive element is associated with development of primary cutaneous lymphoproliferative disorders.
  • Lymphomatoid papulosis is a preneoplastic cutaneous lymphoproliferative disorder characterized by overexpression of CD30, a member of the tumor necrosis factor receptor superfamily.
  • CD30 signaling is known to have an effect on the growth and survival of lymphoid cells.
  • Therefore, we hypothesized that the development of lymphomatoid papulosis and progression to an associated neoplasm such as cutaneous and systemic anaplastic large cell lymphoma may reflect an underlying genetic defect.
  • In this study, we determined that two allelic forms of the CD30 promoter microsatellite repressive element, designated 30M377 and 30M362, are associated with the development of lymphomatoid papulosis and CD30+ lymphomas in lymphomatoid papulosis patients, respectively.
  • These findings suggest that allele-specific differences in the control of CD30 transcription may determine the pathogenesis of the spectrum of CD30+ cutaneous lymphoproliferative disorders.
  • [MeSH-major] Antigens, CD30 / genetics. Lymphoma, Large B-Cell, Diffuse / genetics. Lymphomatoid Papulosis / genetics. Polymorphism, Genetic. Promoter Regions, Genetic

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  • (PMID = 15894695.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50-CA-93683
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD30
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49. Lai R, Rassidakis GZ, Lin Q, Atwell C, Medeiros LJ, Amin HM: Jak3 activation is significantly associated with ALK expression in anaplastic large cell lymphoma. Hum Pathol; 2005 Sep;36(9):939-44
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Jak3 activation is significantly associated with ALK expression in anaplastic large cell lymphoma.
  • In previous studies of anaplastic large cell lymphoma (ALCL), we showed that inhibition of Jak3 down-regulates activated/phosphorylated Stat3 (pStat3), decreases anaplastic lymphoma kinase (ALK) enzymatic activity, and induces cell-cycle arrest and apoptosis in ALK-positive ALCL.
  • These findings implicate Jak3 as playing a significant role in the pathogenesis of ALK-positive ALCL; most likely via Stat3 and ALK activation.
  • To assess this possibility, we used immunohistochemical staining to evaluate the frequency of expression of Jak3 and its activated/phosphorylated form (pJak3) in 48 systemic ALCL tumors included in a tissue microarray. pJak3 was detected in 17 (81%) of 21 ALK-positive tumors, compared with 3 (11%) of 27 ALK-negative tumors (P < .0001, Fisher exact test).
  • pStat3 was present in 12 (86%) of 14 ALK-positive tumors and in 10 (40%) of 25 ALK-negative tumors assessed (P = .0078).
  • Of 12 ALK-positive/pStat3-positive tumors, 8 (67%) expressed pJak3, but none of 10 ALK-negative/pStat3-positive tumors expressed pJak3.
  • We conclude that Jak3 activation is predominantly restricted to ALK-positive ALCL tumors.
  • Most likely, Jak3 collaborates with ALK in activating Stat3, leading to cell survival, cell-cycle progression, and tumor growth.
  • In contrast, the mechanism of Stat3 activation in ALK-negative ALCL tumors appears to be independent of Jak3.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / enzymology. Protein-Tyrosine Kinases / metabolism

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  • (PMID = 16153455.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / JAK3 protein, human; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 2.7.10.2 / Janus Kinase 3
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50. Kotoula V, Bobos M, Kostopoulos I, Kaloutsi V, Koletsa T, Karayannopoulou G, Papadimitriou CS: In situ detection of hTERT variants in anaplastic large cell lymphoma. Leuk Lymphoma; 2006 Aug;47(8):1639-50
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] In situ detection of hTERT variants in anaplastic large cell lymphoma.
  • The expression of hTERT and its isoforms is difficult to assess in lymphoma tissues with the commonly used reverse transcription-polymerase chain reaction (RT-PCR) methods, because non-neoplastic lymphocytes expressing hTERT are always present in the lymphomatous infiltrates.
  • The present study aimed to investigate hTERT mRNA variants in anaplastic large cell lymphoma (ALCL) (n = 38) with in situ hybridization (ISH), along with the immunodetection of hTERT protein.
  • Although all ALCL examined were found positive for hTERT expression with RT-PCR, hTERT mRNAs were identified in 68% of these tumors with ISH, with a higher incidence in the group bearing ALK translocations (10 out of 11; 90.9%) compared to the ALK negative group (17 out of 27; 59.3%) (PPearson's = 0.002).
  • In approximately 50% of cases, only Bplus positive cells were identified, again with a higher incidence in the ALK positive compared to the ALK negative group (PPearson's = 0.016).
  • In conclusion, ISH for hTERT mRNAs appears to be a valuable tool for the investigation of hTERT expression in lymphomas.
  • Aberrations in hTERT variant profiles and a decline in the expression of the B deleted isoform may be associated with the pathogenesis of ALCL, especially with respect to ALK positive tumors.
  • [MeSH-major] Genetic Variation. In Situ Hybridization / methods. Lymphoma, Large-Cell, Anaplastic / genetics. Telomerase / genetics

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  • (PMID = 16966278.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / RNA, Messenger; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase
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51. Lu Y, Zhao X, Wang E, Chen W, Huang Q: ALK-negative anaplastic large cell lymphoma with extensive peripheral blood and bone marrow involvements manifested as "leukemic phase". Leuk Res; 2010 Apr;34(4):475-82
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  • [Title] ALK-negative anaplastic large cell lymphoma with extensive peripheral blood and bone marrow involvements manifested as "leukemic phase".
  • CD30-positive anaplastic large cell lymphoma (ALCL) is a distinctive malignant large cell lymphoma of T-cell lineage, often presenting in lymph node or extranodal sites.
  • ALCL cases with extensive bone marrow and peripheral blood involvement manifested as "leukemic phase" are extremely rare and the most of those cases reported are anaplastic large cell lymphoma kinase (ALK) positive ALCL in childhood population.
  • Here we report four adult cases of ALK-negative ALCL with extensive bone marrow and peripheral blood involvement manifested as "leukemic phase".
  • Circulating large lymphoma cells varied from 20 to 80% in peripheral blood and bone marrow biopsy showed various nodular or interstitial infiltrates.
  • By reviewing the clinicopathologic data of previously reported ALCL cases with extensive bone marrow and peripheral blood involvement, there appears to be of large variations in regard to the patient's age, morphologic variants, immunophenotypic or genotypic characteristics of the disease.
  • While most cases of ALCL with peripheral blood and bone marrow involvement were ALK-positive or carrying t(2;5) translocation, rare ALK-negative cases were also present.
  • Leukemic ALCL patients usually have unfavourable prognosis, regardless of ALK expression.
  • [MeSH-major] Bone Marrow Neoplasms / secondary. Lymphoma, Large-Cell, Anaplastic / pathology. Protein-Tyrosine Kinases / genetics
  • [MeSH-minor] Adult. Disease Progression. Female. Humans. Male. Middle Aged. Neoplasm Invasiveness. Receptor Protein-Tyrosine Kinases

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  • [Copyright] Copyright (c) 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 19695703.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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52. Shimoyama Y, Sakakibara A, Kawai K, Nagasaka T, Nakamura S: Molecular diagnosis of malignant lymphoma: mantle cell lymphoma, anaplastic large cell lymphoma, and marginal zone B-cell lymphoma of malt. Nagoya J Med Sci; 2006 Jan;68(1-2):1-8
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  • [Title] Molecular diagnosis of malignant lymphoma: mantle cell lymphoma, anaplastic large cell lymphoma, and marginal zone B-cell lymphoma of malt.
  • Malignant lymphoma is a heterogeneous category embracing three major types of lymphoid neoplasms: B cell neoplasms, T and NK cell neoplasms, and Hodgkin lymphoma.
  • Within each type, distinct disease entities are defined based on a combination of morphology, immunophenotype, genetic features and clinical syndromes, the emphasis on which represents a new paradigm in the lymphoma classification of the World Health Organization (WHO).
  • These lymphoma entities often have distinctive cytogenetic abnormalities, usually involving translocations that place a potential cellular oncogene under the influence of the immunoglobulin in some low-grade B-cell lymphomas.
  • Both pathologists and oncologists are now concerned with better understanding each disease entity and its spectrum of morphology, genetic events, and clinical behaviors.
  • Over the last decade, significant progress has been made in the molecular characterizations of mantle cell lymphoma, anaplastic large cell lymphoma, and marginal zone B-cell lymphoma of mucosa-associated lymphoid tissue (MALT), which have not only provided insights into the pathogenesis of lymphomas, but also valuable data that could lead to therapies based on their clinical behavior.
  • [MeSH-major] Biomarkers, Tumor / analysis. Lymphoma, B-Cell / diagnosis. Lymphoma, B-Cell, Marginal Zone / diagnosis. Lymphoma, Large-Cell, Anaplastic / diagnosis. Lymphoma, Mantle-Cell / diagnosis. Molecular Diagnostic Techniques

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  • (PMID = 16579170.001).
  • [ISSN] 0027-7622
  • [Journal-full-title] Nagoya journal of medical science
  • [ISO-abbreviation] Nagoya J Med Sci
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / API2-MALT1 fusion protein, human; 0 / Biomarkers, Tumor; 0 / Oncogene Proteins, Fusion; 136601-57-5 / Cyclin D1; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Number-of-references] 23
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53. Yaakup H, Sagap I, Fadilah SA: Primary oesophageal Ki (CD30)-positive ALK+ anaplastic large cell lymphoma of T-cell phenotype. Singapore Med J; 2008 Oct;49(10):e289-92
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  • [Title] Primary oesophageal Ki (CD30)-positive ALK+ anaplastic large cell lymphoma of T-cell phenotype.
  • Primary oesophageal lymphoma is a very rare entity, with fewer than 30 reported cases worldwide.
  • Most of the oesophageal lymphomas are diffuse large B-cell type, with only one reported case of anaplastic large cell lymphoma (ALCL) of T-cell phenotype.
  • Primary oesophageal lymphomas that are not associated with an immunocompromised state tend to affect elderly patients.
  • We describe the first case of primary oesophageal Ki (CD30)-positive ALK+ALCL of T-cell phenotype in a 34-year-old immunocompetent woman, who presented with a two-year history of dysphagia.
  • She was treated with chemotherapy and endoscopic oesophageal dilations and stenting, resulting in complete remission of the lymphoma and resolution of the dysphagia.
  • She then underwent autologous peripheral blood haematopoietic stem cell transplantation and remained disease-free two years after the diagnosis.
  • [MeSH-major] Antigens, CD30 / biosynthesis. Esophageal Neoplasms / metabolism. Esophageal Neoplasms / pathology. Lymphoma, Large-Cell, Anaplastic / metabolism. Lymphoma, Large-Cell, Anaplastic / pathology. Protein-Tyrosine Kinases / biosynthesis
  • [MeSH-minor] Adult. Disease-Free Survival. Endoscopy / methods. Female. Hematopoietic Stem Cell Transplantation / methods. Humans. Phenotype. Receptor Protein-Tyrosine Kinases. Remission Induction. T-Lymphocytes / metabolism. Tomography, X-Ray Computed / methods. Treatment Outcome

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  • (PMID = 18946602.001).
  • [ISSN] 0037-5675
  • [Journal-full-title] Singapore medical journal
  • [ISO-abbreviation] Singapore Med J
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Singapore
  • [Chemical-registry-number] 0 / Antigens, CD30; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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54. Sugiyama H, Asagoe K, Morizane S, Oono T, Okazaki F, Iwatsuki K: Leukocyte common antigen-negative, aggressive cutaneous anaplastic large cell lymphoma with prominent pseudocarcinomatous hyperplasia. Eur J Dermatol; 2008 Jan-Feb;18(1):74-7
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  • [Title] Leukocyte common antigen-negative, aggressive cutaneous anaplastic large cell lymphoma with prominent pseudocarcinomatous hyperplasia.
  • Patients with anaplastic large cell lymphoma (ALCL) often present with tumor-mediated skin changes, including pseudocarcinomatous hyperplasia (PCH), acquired ichthyosis, and tissue neutrophilia.
  • We report a 58-year-old male patient with leukocyte common antigen (LCA)-negative, null cell-type ALCL associated with marked PCH mimicking undifferentiated squamous cell carcinoma.
  • Although lymphocyte markers were lacking, the CD30 expression and the clonal rearrangement of the T-cell receptor gamma gene confirmed the diagnosis of ALCL.
  • The patient had an aggressive clinical course, in which the tumor cells metastasized to the regional lymph nodes a few months after surgical removal of the primary lesion, and skin nodules recurred on the face despite intensive polychemotherapy, followed by autologous peripheral blood stem cell transplantation.
  • The diagnosis of ALCL was delayed in our case because of the prominent PCH, the lack of LCA, and the unusually rapid progression of the tumor.
  • [MeSH-major] Antigens, CD45 / analysis. Lymphoma, Large-Cell, Anaplastic / pathology. Nose Neoplasms / pathology. Skin Neoplasms / pathology
  • [MeSH-minor] Carcinoma, Squamous Cell / diagnosis. Diagnosis, Differential. Humans. Hyperplasia. Lymphatic Metastasis. Male. Middle Aged


55. Watanabe M, Ogawa Y, Itoh K, Koiwa T, Kadin ME, Watanabe T, Okayasu I, Higashihara M, Horie R: Hypomethylation of CD30 CpG islands with aberrant JunB expression drives CD30 induction in Hodgkin lymphoma and anaplastic large cell lymphoma. Lab Invest; 2008 Jan;88(1):48-57
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  • [Title] Hypomethylation of CD30 CpG islands with aberrant JunB expression drives CD30 induction in Hodgkin lymphoma and anaplastic large cell lymphoma.
  • High expression of CD30 and JunB is the hallmark of malignant cells in Hodgkin lymphoma (HL) and anaplastic large cell lymphoma (ALCL).
  • Ligand-independent signaling by CD30 induces JunB, which activates the CD30 promoter, stabilizing CD30 expression and supporting the survival of Hodgkin-Reed-Sternberg (H-RS) and ALCL cells.
  • Here we show for the first time CpG islands encompassing 60 CpG dinucleotides, located in the core promoter, exon 1 and intron 1 of CD30 gene.
  • Analysis of the methylation status of CD30 CpG islands in H-RS, ALCL and unrelated cell lines reveals an inverse relationship between the extent of CD30 CpG methylation and CD30 expression.
  • CD30 CpG islands of H-RS and ALCL cell lines are rarely methylated.
  • Methylation of the CD30 promoter decreases CD30 induction and JunB action on the demethylated CD30 promoter enhances CD30 induction.
  • CD30 and JunB are strongly expressed in H-RS and ALCL cells, whereas they are not expressed in nonmalignant lymphocytes in which CD30 CpG islands are rarely methylated.
  • We conclude that constitutive action of aberrantly expressed JunB on hypomethylated CD30 CpG islands of lymphocytes triggers CD30 induction and initiates activation of the JunB-CD30-JunB loop, essential to the pathogenesis of HL and ALCL.
  • [MeSH-major] Antigens, CD30 / biosynthesis. CpG Islands. DNA Methylation. Hodgkin Disease / immunology. Lymphoma, Large-Cell, Anaplastic / immunology. Proto-Oncogene Proteins c-jun / metabolism
  • [MeSH-minor] Base Sequence. Blotting, Northern. Cell Line. DNA. DNA Primers. Humans. Immunohistochemistry. Molecular Sequence Data. Promoter Regions, Genetic. Reverse Transcriptase Polymerase Chain Reaction


56. Rodig SJ, Ouyang J, Juszczynski P, Currie T, Law K, Neuberg DS, Rabinovich GA, Shipp MA, Kutok JL: AP1-dependent galectin-1 expression delineates classical hodgkin and anaplastic large cell lymphomas from other lymphoid malignancies with shared molecular features. Clin Cancer Res; 2008 Jun 1;14(11):3338-44
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  • [Title] AP1-dependent galectin-1 expression delineates classical hodgkin and anaplastic large cell lymphomas from other lymphoid malignancies with shared molecular features.
  • We recently found that Reed-Sternberg cell Gal1 promotes the immunosuppressive T-helper 2/T-regulatory cell-skewed microenvironment in classical Hodgkin lymphoma (cHL).
  • In addition, because there are common signaling and survival pathways in cHL and additional non-Hodgkin lymphomas, we also evaluated whether the AP1/Gal1 signature is shared by other molecularly or morphologically related lymphomas.
  • EXPERIMENTAL DESIGN: We evaluated 225 cases of primary cHL and non-Hodgkin lymphoma for evidence of a functional AP1/Gal1 signature by immunohistochemical techniques.
  • In contrast, diffuse large B-cell lymphoma, primary mediastinal large B-cell lymphoma, and another Hodgkin-related entity, nodular lymphocyte-predominant Hodgkin lymphoma, do not express Gal1.
  • However, anaplastic large cell lymphoma (ALCL), consistently expresses both Gal1 and its transcriptional regulator, c-Jun.
  • The presence of activated c-Jun, indicative of functional AP1 activity, was confirmed by phospho-c-Jun immunostaining in cHL and ALCL.
  • CONCLUSIONS: These findings establish a functional AP1 signature that includes Gal1 expression in cHL and ALCL and suggests a common mechanism for tumor immunotolerance in these diseases.
  • In addition, the combination of Gal1 and c-Jun serve as diagnostic biomarkers that delineate cHL and ALCL from other lymphomas with shared morphologic and/or molecular features.
  • [MeSH-major] Biomarkers, Tumor / analysis. Galectin 1 / biosynthesis. Hodgkin Disease / metabolism. Lymphoma, Large-Cell, Anaplastic / metabolism. Lymphoproliferative Disorders / metabolism. Transcription Factor AP-1 / metabolism
  • [MeSH-minor] Diagnosis, Differential. Gene Expression. Humans. Immunohistochemistry. Proto-Oncogene Proteins c-jun / metabolism. Reed-Sternberg Cells / metabolism

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  • (PMID = 18519761.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Galectin 1; 0 / Proto-Oncogene Proteins c-jun; 0 / Transcription Factor AP-1
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57. Li JF, Li GD, Gu L, Liu WP, Li FY, Liao DY, Ma ZG: [Study on activation of AKT/mTOR pathway in anaplastic large cell lymphoma]. Zhonghua Xue Ye Xue Za Zhi; 2008 Oct;29(10):649-53
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  • [Title] [Study on activation of AKT/mTOR pathway in anaplastic large cell lymphoma].
  • OBJECTIVE: To study the expression of anaplastic lymphoma kinase (ALK) and the phosphorylation status of AKT, mammalian target of rapamycin (mTOR), 4E-binding protein 1 (4E-BP1) and ribosomal protein S6 kinase (p70S6K) and their interrelationships and clinical pathological significance in anaplastic large cell lymphoma (ALCL) patients.
  • RESULTS: Among the 81 ALCL patients, 51 (63.0%) expressed ALK, whereas the other 30 (37.0%) did not.
  • Patients with ALK(+) ALCL had a better prognosis than those with ALK-ALCL (P < 0.05).
  • Out of the 71 ALCL samples studied, p-AKT was detected in 54 (76.1%) samples and its phosphorylation was correlated with ALK expression (P < 0.05); p-mTOR was detected in 57 (80.3%) samples and its expression was correlated with both ALK and p-AKT (P < 0.05); p-4E-BP1 and p-p70S6K were detected in 64 (90.1%) and 66 (93.0%) samples respectively, and their expressions were related with p-mTOR (P < 0.05), but not with ALK or p-AKT (P > 0.05).
  • CONCLUSION: Expressions of p-AKT, p-mTOR, p-4E-BP1 and p-p70S6K are detected in ALCL, while ALK(+) cases have higher incidence than those with ALK(-) cases.
  • Phosphorylation of AKT and mTOR is correlated with ALK expression, suggesting that there is an activated pathway of AKT/mTOR in patients with ALK(+) ALCL, but the activation have no obvious prognostic significance.
  • [MeSH-major] Intracellular Signaling Peptides and Proteins / metabolism. Lymphoma, Large-Cell, Anaplastic / metabolism. Protein-Serine-Threonine Kinases / metabolism. Protein-Tyrosine Kinases / metabolism. Proto-Oncogene Proteins c-akt / metabolism

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  • (PMID = 19176054.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / EIF4EBP1 protein, human; 0 / Intracellular Signaling Peptides and Proteins; 0 / Phosphoproteins; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.1 / Ribosomal Protein S6 Kinases, 70-kDa
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58. Mathas S, Kreher S, Meaburn KJ, Jöhrens K, Lamprecht B, Assaf C, Sterry W, Kadin ME, Daibata M, Joos S, Hummel M, Stein H, Janz M, Anagnostopoulos I, Schrock E, Misteli T, Dörken B: Gene deregulation and spatial genome reorganization near breakpoints prior to formation of translocations in anaplastic large cell lymphoma. Proc Natl Acad Sci U S A; 2009 Apr 7;106(14):5831-6
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  • [Title] Gene deregulation and spatial genome reorganization near breakpoints prior to formation of translocations in anaplastic large cell lymphoma.
  • We used anaplastic large cell lymphoma (ALCL) with and without the characteristic t(2;5)(p23;q35) translocation to study the mechanisms of formation of translocations and of ALCL transformation.
  • We report deregulation of several genes located near the ALCL translocation breakpoint, regardless of whether the tumor contains the t(2;5).
  • Their up-regulation promotes cell survival and repression of T cell-specific gene expression programs that are characteristic for ALCL.
  • The deregulated genes are in spatial proximity within the nuclear space of t(2;5)-negative ALCL cells, facilitating their translocation on induction of double-strand breaks.
  • Also, our data demonstrate that deregulation of breakpoint-proximal genes has a key role in ALCL.

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  • (PMID = 19321746.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / FOSL2 protein, human; 0 / Fos-Related Antigen-2; 0 / ID2 protein, human; 0 / Inhibitor of Differentiation Protein 2; EC 2.7.10.1 / Receptor, Macrophage Colony-Stimulating Factor
  • [Other-IDs] NLM/ PMC2667034
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59. Wright CW, Rumble JM, Duckett CS: CD30 activates both the canonical and alternative NF-kappaB pathways in anaplastic large cell lymphoma cells. J Biol Chem; 2007 Apr 6;282(14):10252-62
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  • [Title] CD30 activates both the canonical and alternative NF-kappaB pathways in anaplastic large cell lymphoma cells.
  • CD30 is a member of the tumor necrosis factor receptor superfamily whose expression is up-regulated on anaplastic large cell lymphoma (ALCL) and Hodgkin lymphoma (HL) cells.
  • Many different outcomes of CD30 stimulation have been reported, including cell cycle arrest, apoptosis, and activation of the prosurvival transcription factor, NF-kappaB, although this last activity is much less well defined in ALCL cells.
  • In order to better understand the signaling properties of CD30 in cancer, we established a system for the stimulation of CD30 with its physiological ligand.
  • Using this system, CD30 was stimulated on ALCL and HL cells, and the subsequent CD30 signaling properties were characterized.
  • We show that a fraction of ALCL cells rapidly underwent apoptosis following CD30 stimulation, whereas HL cells were unaffected.
  • The surviving ALCL cells exhibited robust activation of both the canonical and alternative NF-kappaB pathways as measured by nuclear translocation of RelA, p50, RelB, and p52, and this culminated in the transactivation of classical NF-kappaB-responsive genes.
  • With prolonged CD30 stimulation, ALCL cells underwent cell cycle arrest that correlated with expression of the cell cycle inhibitor p21(waf1).
  • Furthermore, p21(waf1) expression and cell cycle arrest were found to depend predominantly on the canonical NF-kappaB pathway, since it was reversed by RNA interference-mediated suppression of RelA.
  • These data reveal that in ALCL cells, in contrast to other cell types, CD30 stimulation elicits p21(waf1)-mediated arrest through the canonical but not the alternative NF-kappaB pathway.
  • [MeSH-major] Antigens, CD30 / metabolism. CD30 Ligand / metabolism. Hodgkin Disease / metabolism. Lymphoma, Large B-Cell, Diffuse / metabolism. NF-kappa B / metabolism. Signal Transduction
  • [MeSH-minor] Active Transport, Cell Nucleus / drug effects. Active Transport, Cell Nucleus / genetics. Animals. CHO Cells. Cell Cycle / drug effects. Cell Cycle / genetics. Cell Line, Tumor. Cell Nucleus / genetics. Cell Nucleus / metabolism. Cell Survival / drug effects. Cell Survival / genetics. Cricetinae. Cricetulus. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Humans. RNA Interference / drug effects

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  • (PMID = 17261581.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / GM067827; United States / NIAID NIH HHS / AI / T32 AI007413-12; United States / NHLBI NIH HHS / HL / T32 HL07517
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / CD30 Ligand; 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / NF-kappa B; 0 / TNFSF8 protein, human
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60. Rapkiewicz A, Wen H, Sen F, Das K: Cytomorphologic examination of anaplastic large cell lymphoma by fine-needle aspiration cytology. Cancer; 2007 Dec 25;111(6):499-507
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  • [Title] Cytomorphologic examination of anaplastic large cell lymphoma by fine-needle aspiration cytology.
  • BACKGROUND: The cytomorphology of anaplastic large cell lymphoma (ALCL) is distinctive yet variable.
  • To the authors' knowledge, to date only small case series have described the cytologic findings noted in patients with ALCL.
  • The current series is the largest case series presented to date to retrospectively review the cytomorpholgic findings noted in patients with ALCL, with specific attention paid to those with anaplastic lymphoma kinase (ALK)-negative ALCL.
  • METHODS: Over a 13-year period, the available Diff-Quik cytology smears and surgical excision specimens taken from patients with ALCL were evaluated.
  • Different clinical and morphologic parameters were evaluated, including ALK status.
  • ALK-negative ALCL cytology smears were found to have a high number of anaplastic cells compared with ALK-positive cases.
  • CONCLUSIONS: ALCL can be diagnosed accurately by fine-needle aspiration cytology (FNAC) alone when aided by immunocytochemistry in ALK-positive cases.
  • Ancillary studies should be anticipated such that material for cell block preparation and molecular studies is taken at the time of FNAC.
  • The results of the current study demonstrate the varied FNAC morphology of ALCL.
  • [MeSH-major] Biopsy, Fine-Needle. Lymphoma, Large-Cell, Anaplastic / pathology

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  • [Copyright] 2007 American Cancer Society
  • (PMID = 17941004.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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61. Siordia-Reyes AG, Ferman-Cano F, Rodríguez-Velasco A: [ALK-1 positive anaplastic large cell lymphoma of the lung. Report of a pediatric case]. Gac Med Mex; 2005 Nov-Dec;141(6):531-4
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  • [Title] [ALK-1 positive anaplastic large cell lymphoma of the lung. Report of a pediatric case].
  • [Transliterated title] Linfoma anaplásico de células grandes ALK-1 positivo, primario de pulmón. Informe de un caso pediátrico.
  • Ki-1 anaplastic large cell non-Hodgkin lymphoma is a well recognized clinical entity.
  • In the extranodal disease, which occurs in approximately half of the cases, the skin is the most common site; bone marrow, lung and central nervous system are generally not involved.
  • Anaplastic large cell lymphoma is more common among young people, in whom the prognosis is more favorable.
  • Primary anaplastic large cell lymphoma of the lung is a rare clinical entity.
  • Its clinical expression is similar to a high grade malignant lymphoma, and in most cases the diagnosis is made in advanced stages.
  • We present a pediatric case with ALK-1 positive anaplastic large cell lymphoma of the lung.
  • [MeSH-major] Lung Neoplasms / chemistry. Lymphoma, Large B-Cell, Diffuse / chemistry. Membrane Proteins / analysis
  • [MeSH-minor] Activin Receptors, Type II. Child. Humans. Male

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  • (PMID = 16381509.001).
  • [ISSN] 0016-3813
  • [Journal-full-title] Gaceta médica de México
  • [ISO-abbreviation] Gac Med Mex
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Mexico
  • [Chemical-registry-number] 0 / Membrane Proteins; EC 2.7.11.30 / ACVRL1 protein, human; EC 2.7.11.30 / Activin Receptors, Type II
  • [Number-of-references] 16
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62. Li JF, Li GD, Liu WP, Wang Y, Cheng JR, Chen Y, Yang H, Tang HL, Bai YQ, Lin DG, DU LH, Peng FX, Yang YH, Zhao C: [Expression of anaplastic lymphoma kinase and survivin proteins in anaplastic large cell lymphoma and its significance]. Zhonghua Bing Li Xue Za Zhi; 2006 Apr;35(4):213-7
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  • [Title] [Expression of anaplastic lymphoma kinase and survivin proteins in anaplastic large cell lymphoma and its significance].
  • OBJECTIVE: To study the expression of anaplastic lymphoma kinase (ALK) and survivin proteins in anaplastic large cell lymphoma (ALCL) and there clinical significance.
  • METHODS: The morphologic characteristics were studied by routine light microscopy.
  • RESULTS: ALK protein was positive in 51 cases (63%) and negative in 30 cases (37%) of the 81 cases of ALCL studied.
  • As for survivin protein, there were various degrees of expression in all the 77 ALCL cases studied.
  • CONCLUSION: Survivin protein expression can serve as an independent prognostic predictor of unfavorable clinical outcome in patients with ALCL, especially when ALK protein is positive.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / metabolism. Microtubule-Associated Proteins / metabolism. Neoplasm Proteins / metabolism. Protein-Tyrosine Kinases / metabolism

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  • (PMID = 16776978.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Biomarkers, Tumor; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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63. Schumacher JA, Crockett DK, Elenitoba-Johnson KS, Lim MS: Proteome-wide changes induced by the Hsp90 inhibitor, geldanamycin in anaplastic large cell lymphoma cells. Proteomics; 2007 Aug;7(15):2603-16
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  • [Title] Proteome-wide changes induced by the Hsp90 inhibitor, geldanamycin in anaplastic large cell lymphoma cells.
  • The molecular chaperone heat shock protein 90 (Hsp90) affects the function of many oncogenic signaling proteins including nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) expressed in anaplastic large cell lymphoma (ALCL).
  • While ALK-positive ALCL cells are sensitive to the Hsp90 inhibitor and the geldanamycin (GA) analog, 17-allylamino-17-demethoxygeldanamycin (17-AAG), the proteomic effects of these drugs on ALK-positive ALCL cells are unpublished.
  • In this study, we investigated the cellular, biologic, and proteomic changes occurring in ALK-positive ALCL cells in response to GA treatment.
  • GA induced G2/M cell cycle arrest and caspase-3-mediated apoptosis.
  • Our studies reveal some of the molecular and proteomic consequences of Hsp90 inhibition in ALK-positive ALCL cells and provide novel insights into the mechanisms of its diverse cellular effects.
  • [MeSH-major] Antibiotics, Antineoplastic / pharmacology. Benzoquinones / pharmacology. Enzyme Inhibitors / pharmacology. HSP90 Heat-Shock Proteins / antagonists & inhibitors. Lactams, Macrocyclic / pharmacology. Lymphoma, Large B-Cell, Diffuse / metabolism. Proteome / analysis
  • [MeSH-minor] Apoptosis / drug effects. Apoptosis / physiology. Caspase 3 / metabolism. Cell Cycle / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. DNA, Neoplasm / analysis. Humans. Models, Biological. Reproducibility of Results

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  • (PMID = 17610208.001).
  • [ISSN] 1615-9853
  • [Journal-full-title] Proteomics
  • [ISO-abbreviation] Proteomics
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Benzoquinones; 0 / DNA, Neoplasm; 0 / Enzyme Inhibitors; 0 / HSP90 Heat-Shock Proteins; 0 / Lactams, Macrocyclic; 0 / Proteome; EC 3.4.22.- / Caspase 3; Z3K3VJ16KU / geldanamycin
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64. Hirsch B, Hummel M, Bentink S, Fouladi F, Spang R, Zollinger R, Stein H, Dürkop H: CD30-induced signaling is absent in Hodgkin's cells but present in anaplastic large cell lymphoma cells. Am J Pathol; 2008 Feb;172(2):510-20
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  • [Title] CD30-induced signaling is absent in Hodgkin's cells but present in anaplastic large cell lymphoma cells.
  • High CD30 expression in classical Hodgkin's lymphoma and anaplastic large cell lymphoma (ALCL) suggests an important pathogenic role of this cytokine receptor.
  • To test this hypothesis, we investigated CD30 signaling in Hodgkin's and ALCL cell lines by different approaches:.
  • 1) CD30 stimulation, 2) CD30 down-regulation, and 3) a combination of both.
  • We demonstrate that Hodgkin's cells are virtually CD30 unresponsive.
  • Neither CD30 stimulation nor CD30 silencing of Hodgkin's cells had any significant effect.
  • In contrast, CD30 stimulation of ALCL cells activated nuclear transcription factor-kappaB (NF-kappaB), induced major transcriptional changes, and decreased proliferation.
  • These effects could be abrogated by down-regulation of CD30.
  • Stimulation of CD30 in ALCL cells, stably transfected with a dominant-negative NF-kappaB inhibitor, induced pronounced caspase activation and massive apoptosis.
  • Our data indicate that 1) CD30 signaling is not effective in Hodgkin's cell lines but is effective in ALCL cell lines, 2) CD30 is probably not significantly involved in the pathogenesis of classical Hodgkin's lymphoma, and 3) CD30 stimulation triggers two competing effects in ALCL cells, namely activation of caspases and NF-kappaB-mediated survival.
  • These data suggest that CD30-targeted therapy in ALCL should be combined with NF-kappaB inhibitors to induce effective cell killing.
  • [MeSH-major] Antigens, CD30 / metabolism. Gene Expression Regulation, Neoplastic. Hodgkin Disease / metabolism. Lymphoma, Large-Cell, Anaplastic / metabolism. Signal Transduction / physiology
  • [MeSH-minor] Apoptosis / physiology. Caspases / metabolism. Cell Line, Tumor. Cell Proliferation. Electrophoretic Mobility Shift Assay. Enzyme Activation / physiology. Flow Cytometry. Gene Expression. Gene Expression Profiling. Humans. Immunoblotting. NF-kappa B / metabolism. Oligonucleotide Array Sequence Analysis. RNA, Small Interfering. Reverse Transcriptase Polymerase Chain Reaction. Transfection

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  • (PMID = 18187570.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / NF-kappa B; 0 / RNA, Small Interfering; EC 3.4.22.- / Caspases
  • [Other-IDs] NLM/ PMC2312360
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65. Georgakis GV, Li Y, Rassidakis GZ, Medeiros LJ, Younes A: The HSP90 inhibitor 17-AAG synergizes with doxorubicin and U0126 in anaplastic large cell lymphoma irrespective of ALK expression. Exp Hematol; 2006 Dec;34(12):1670-9
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  • [Title] The HSP90 inhibitor 17-AAG synergizes with doxorubicin and U0126 in anaplastic large cell lymphoma irrespective of ALK expression.
  • OBJECTIVE: Heat shock protein 90 (HSP90) chaperones and maintains the molecular integrity of a variety of signal transduction proteins, including the nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) oncogenic protein, a genetic abnormality that is frequently observed in anaplastic large cell lymphoma (ALCL) cells.
  • Here we demonstrate that HSP90 is overexpressed in primary and cultured ALK-positive and ALK-negative ALCL cells, and we evaluate the potential role of the small molecule inhibitor of HSP90, 17-allylamino-17-demethoxygeldanamycin (17-AAG) in treating ALCL.
  • Apoptosis and cell-cycle arrest were determined by Annexin-V/propidium iodide and propidium iodide staining, respectively, and fluorescein-activated cell sorting analysis.
  • RESULTS: Treatment of cultured ALCL cells with 17-AAG induced cell-cycle arrest and apoptosis, irrespective of ALK expression.
  • At the molecular level, 17-AAG induced degradation of ALK and Akt proteins, dephosphorylated extracellular signal-regulated kinase, and degraded the cell-cycle regulatory protein cyclin D1 and its cyclin-dependent kinases, CDK4 and CDK6, but had a differential effect on p27 and p53 proteins.
  • Inhibition of extracellular signal-regulated kinase phosphorylation by the mitogen activated protein kinase inhibitor U0126 induced cell death in all ALCL cell lines, and sublethal concentration 17-AAG showed synergistic antiproliferative effects when combined with U0126 or doxorubicin.
  • CONCLUSION: Our data demonstrate that targeting HSP90 function by 17-AAG may offer a novel therapeutic strategy for ALCL, either as single-agent activity or by combining 17-AAG with conventional or targeted therapeutic schemes.
  • [MeSH-major] Benzoquinones / pharmacology. Butadienes / pharmacology. Doxorubicin / pharmacology. HSP90 Heat-Shock Proteins / antagonists & inhibitors. Lactams, Macrocyclic / pharmacology. Lymphoma, Large-Cell, Anaplastic / metabolism. Nitriles / pharmacology. Protein-Tyrosine Kinases / biosynthesis
  • [MeSH-minor] Apoptosis / drug effects. Caspase 3 / drug effects. Caspase 3 / metabolism. Cell Line, Tumor. Cell Proliferation / drug effects. Cyclin D. Cyclin-Dependent Kinase 4 / drug effects. Cyclin-Dependent Kinase 4 / metabolism. Cyclin-Dependent Kinase 6 / drug effects. Cyclin-Dependent Kinase 6 / metabolism. Cyclins / drug effects. Cyclins / metabolism. Dose-Response Relationship, Drug. Down-Regulation / drug effects. Drug Synergism. Extracellular Signal-Regulated MAP Kinases / drug effects. Extracellular Signal-Regulated MAP Kinases / metabolism. G0 Phase / drug effects. G1 Phase / drug effects. Humans. Mitogen-Activated Protein Kinase 1 / drug effects. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / drug effects. Mitogen-Activated Protein Kinase 3 / metabolism. Phosphorylation. Receptor Protein-Tyrosine Kinases. Time Factors

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  • (PMID = 17157164.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Benzoquinones; 0 / Butadienes; 0 / Cyclin D; 0 / Cyclins; 0 / HSP90 Heat-Shock Proteins; 0 / Lactams, Macrocyclic; 0 / Nitriles; 0 / U 0126; 4GY0AVT3L4 / tanespimycin; 80168379AG / Doxorubicin; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 2.7.11.22 / CDK4 protein, human; EC 2.7.11.22 / CDK6 protein, human; EC 2.7.11.22 / Cyclin-Dependent Kinase 4; EC 2.7.11.22 / Cyclin-Dependent Kinase 6; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 3.4.22.- / Caspase 3
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66. Krysov SV, Rowley TF, Al-Shamkhani A: Inhibition of p38 mitogen-activated protein kinase unmasks a CD30-triggered apoptotic pathway in anaplastic large cell lymphoma cells. Mol Cancer Ther; 2007 Feb;6(2):703-11
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  • [Title] Inhibition of p38 mitogen-activated protein kinase unmasks a CD30-triggered apoptotic pathway in anaplastic large cell lymphoma cells.
  • CD30, a non-death domain-containing member of the tumor necrosis factor receptor superfamily, triggers apoptosis in anaplastic large cell lymphoma cells.
  • The CD30 signaling pathways that lead to the induction of apoptosis are poorly defined.
  • Here, we show that the induction of apoptosis by CD30 requires concurrent inhibition of p38 mitogen-activated protein kinase, which itself is activated by engagement of CD30 with CD30 ligand.
  • Treatment of anaplastic large cell lymphoma cells with CD30 ligand and pharmacologic inhibitors of p38 mitogen-activated protein kinase, but not with CD30 ligand or inhibitors alone, triggered the activation of caspase-8 and the induction of apoptosis.
  • Importantly, we show that expression of the caspase-8 inhibitor c-FLIP(S) is strongly induced by the CD30 ligand, and that this is dependent on the activation of p38 mitogen-activated protein kinase.
  • Thus, we provide evidence that the induction of apoptosis by CD30 in anaplastic large cell lymphoma cells is normally circumvented by the activation of p38 mitogen-activated protein kinase.
  • These findings have implications for CD30-targeted immunotherapy of anaplastic large cell lymphoma.
  • [MeSH-major] Antigens, CD30 / pharmacology. Apoptosis / drug effects. Lymphoma, Large-Cell, Anaplastic / metabolism. p38 Mitogen-Activated Protein Kinases / antagonists & inhibitors
  • [MeSH-minor] Antigens, CD95 / metabolism. Blotting, Western. CASP8 and FADD-Like Apoptosis Regulating Protein / metabolism. Caspase 3 / metabolism. Caspase 8 / metabolism. Caspase Inhibitors. Cell Cycle / drug effects. Fas Ligand Protein / metabolism. Fas-Associated Death Domain Protein / metabolism. Humans. Receptors, TNF-Related Apoptosis-Inducing Ligand / metabolism. Receptors, Tumor Necrosis Factor / metabolism. Receptors, Tumor Necrosis Factor, Member 25 / metabolism. Receptors, Tumor Necrosis Factor, Type I / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Transfection. Tumor Cells, Cultured / drug effects. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 17308066.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Antigens, CD95; 0 / CASP8 and FADD-Like Apoptosis Regulating Protein; 0 / CFLAR protein, human; 0 / Caspase Inhibitors; 0 / Fas Ligand Protein; 0 / Fas-Associated Death Domain Protein; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / Receptors, Tumor Necrosis Factor; 0 / Receptors, Tumor Necrosis Factor, Member 25; 0 / Receptors, Tumor Necrosis Factor, Type I; 0 / TNFRSF10A protein, human; 0 / TNFRSF25 protein, human; 0 / Tumor Necrosis Factor-alpha; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 8
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67. Feldman AL, Law ME, Inwards DJ, Dogan A, McClure RF, Macon WR: PAX5-positive T-cell anaplastic large cell lymphomas associated with extra copies of the PAX5 gene locus. Mod Pathol; 2010 Apr;23(4):593-602

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] PAX5-positive T-cell anaplastic large cell lymphomas associated with extra copies of the PAX5 gene locus.
  • Cell lineage is the major criterion by which lymphomas are classified.
  • Immunohistochemistry has greatly facilitated lymphoma diagnosis by detecting expression of lineage-associated antigens.
  • Anaplastic large cell lymphoma is a T-cell lymphoma that shows morphologic and phenotypic overlap with classical Hodgkin's lymphoma, which is a tumor of B-cell derivation.
  • Staining for the B-cell transcription factor, paired box 5 (PAX5), has been suggested to be helpful in this differential, as it is positive in most classical Hodgkin's lymphomas, but absent in anaplastic large cell lymphomas.
  • In this study we report four systemic T-cell anaplastic large cell lymphomas that were positive for PAX5 by immunohistochemistry, with weak staining intensity similar to that observed in classical Hodgkin's lymphoma.
  • All diagnoses were confirmed by a combination of morphologic, phenotypic, and molecular criteria.
  • Three cases were anaplastic lymphoma kinase (ALK) negative and one was ALK positive.
  • PAX5 immunohistochemistry was negative in 198 additional peripheral T-cell lymphomas, including 66 anaplastic large cell lymphomas.
  • Unexpectedly, although PAX5 translocations were absent, all evaluable PAX5-positive anaplastic large cell lymphomas showed extra copies of the PAX5 gene locus by fluorescence in situ hybridization (FISH).
  • In contrast, only 4% of PAX5-negative peripheral T-cell lymphomas had extra copies of PAX5.
  • We conclude that aberrant expression of PAX5 occurs rarely in T-cell anaplastic large cell lymphomas, and may be associated with extra copies of the PAX5 gene.
  • PAX5-positive lymphomas with morphologic features overlapping different lymphoma types should be evaluated with an extensive immunohistochemical panel and/or molecular studies to avoid diagnostic errors that could lead to inappropriate treatment.
  • As PAX5 overexpression causes T-cell neoplasms in experimental models, PAX5 may have contributed to lymphomagenesis in our cases.

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  • (PMID = 20118907.001).
  • [ISSN] 1530-0285
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA097274-08; United States / NCI NIH HHS / CA / P50 CA097274; United States / NCI NIH HHS / CA / P50 CA097274-08
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / B-Cell-Specific Activator Protein; 0 / PAX5 protein, human
  • [Other-IDs] NLM/ NIHMS167829; NLM/ PMC2848697
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68. Pinter-Brown LC: SGN-30: a basis for the effective treatment of CD30 positive hematopoietic malignancies. Expert Opin Investig Drugs; 2008 Dec;17(12):1883-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] SGN-30: a basis for the effective treatment of CD30 positive hematopoietic malignancies.
  • BACKGROUND: Patients with high-risk, relapsed or refractory Hodgkin lymphoma, those with systemic anaplastic large-cell lymphoma, and those with primary cutaneous CD30-positive disorders are in need of novel therapies.
  • CD30, a common marker in these malignancies, is a reasonable immunologic target given its restricted expression in normal states.
  • SGN-30 is a chimeric antibody targeting CD30.
  • The highest response rate was seen in patients with primary cutaneous CD30-positive lymphoproliferative disease and encouraging results were seen in patients with relapsed or refractory systemic anaplastic large-cell lymphoma.
  • Most responses in Hodgkin lymphoma were stable disease.
  • Despite a majority of patients having had stem cell transplantation, the drug was well tolerated.
  • [MeSH-major] Antibodies, Monoclonal / immunology. Antibodies, Monoclonal / therapeutic use. Antigens, CD30 / immunology. Hematologic Neoplasms / drug therapy. Hematologic Neoplasms / immunology. Immunotherapy

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  • (PMID = 19012503.001).
  • [ISSN] 1744-7658
  • [Journal-full-title] Expert opinion on investigational drugs
  • [ISO-abbreviation] Expert Opin Investig Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD30; 0 / SGN-30 monoclonal antibody
  • [Number-of-references] 21
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69. Belloni-Fortina A, Montesco MC, Piaserico S, Bordignon M, Tona F, Feltrin G, Alaibac M: Primary cutaneous CD30+ anaplastic large cell lymphoma in a heart transplant patient: case report and literature review. Acta Derm Venereol; 2009;89(1):74-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary cutaneous CD30+ anaplastic large cell lymphoma in a heart transplant patient: case report and literature review.
  • The risk of a post-transplant lymphoproliferative disorder is 28-49 times the risk of a lymphoproliferative disorder in the normal population.
  • Most cases are of B-cell phenotype and are associated with Epstein-Barr virus infection.
  • Post-transplant lymphoproliferative disorders presenting clinically in the skin are rare and usually of B-cell phenotype.
  • Only rare cases of cutaneous T-cell post-transplant lymphoproliferative disorder have been reported previously, mostly mycosis fungoides type.
  • We describe here a rare primary cutaneous T-cell lymphoma CD30+ arising in a heart transplant patient who had a nodule on the right leg, several years after heart transplantation.
  • The morphology and immunohistochemical findings were consistent with a CD30+ anaplastic large cell lymphoma with a T-cell phenotype.
  • In this patient, the presence of a solitary lesion and the lack of systemic involvement represented the main factors taken into account in choosing the therapy and the patient was therefore treated using a non-aggressive approach, although with systemic immunosuppression.
  • In conclusion, the diagnosis of a CD30+ anaplastic large cell lymphoma in transplant recipients does not imply aggressive clinical behaviour by the lymphoma.
  • [MeSH-major] Antigens, CD30 / analysis. Heart Transplantation. Lymphoma, T-Cell, Cutaneous / etiology. Skin Neoplasms / etiology


70. Hsu FY, Johnston PB, Burke KA, Zhao Y: The expression of CD30 in anaplastic large cell lymphoma is regulated by nucleophosmin-anaplastic lymphoma kinase-mediated JunB level in a cell type-specific manner. Cancer Res; 2006 Sep 15;66(18):9002-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The expression of CD30 in anaplastic large cell lymphoma is regulated by nucleophosmin-anaplastic lymphoma kinase-mediated JunB level in a cell type-specific manner.
  • Chromosomal translocation t(2;5) and the resulting fusion protein nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) are detected in 50% to 70% of anaplastic large cell lymphoma (ALCL), which is a T/null cell non-Hodgkin's lymphoma showing anaplastic morphology with cell surface expression of CD30.
  • Because aberrant CD30 expression was also observed in the T-cell lymphoma derived from lineage-specific NPM-ALK transgenic mice, we tested the hypothesis that there might be a functional relationship between the two neoplastic-related proteins: NPM-ALK and CD30.
  • In this study, we used the RNA interference method to modulate NPM-ALK protein expression in ALCL-derived, t(2;5)-positive Karpas 299 cells.
  • We observed decreased CD30 expression when NPM-ALK was repressed.
  • Further analysis suggested that JunB functioned as the mediator of NPM-ALK-derived CD30 transcriptional regulation.
  • The NPM-ALK-repressed cells, which had low CD30 expression, were characterized with lower cell proliferation compared with cells in the control group, suggesting that altered CD30 expression may correlate to NPM-ALK-mediated tumor cell growth inhibition.
  • Combination of NPM-ALK repression and CD30 ligand leads to significantly increased tumor cell growth inhibition compared with one method alone, suggesting its potential application for ALCL-specific cancer treatment.
  • [MeSH-major] Antigens, CD30 / biosynthesis. Lymphoma, Large B-Cell, Diffuse / metabolism. Protein-Tyrosine Kinases / metabolism. Proto-Oncogene Proteins c-jun / metabolism
  • [MeSH-minor] Cell Growth Processes / physiology. Cell Line, Tumor. Down-Regulation. Gene Expression Regulation, Neoplastic. Gene Silencing. Humans. RNA Interference. RNA, Small Interfering / genetics. Transcription, Genetic. Transcriptional Activation. Transfection

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  • (PMID = 16982741.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA59318
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Proto-Oncogene Proteins c-jun; 0 / RNA, Small Interfering; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases
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71. Kovrigina AM, Probatova NA: [Diagnosis of anaplastic large-cell lymphoma]. Arkh Patol; 2005 Nov-Dec;67(6):7-13
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Diagnosis of anaplastic large-cell lymphoma].
  • Principles of morphological diagnosis of anaplastic large-cell lymphoma (ALCL) are considered, several its variants are distinguished: classic (32 cases), small-cell (4 cases), rich in granulocytes (2 cases) and lymphohistiocytic (1 case).
  • Morphological similarities between ALCL, classic variants of Hodgkin's lymphoma, variants of diffuse large B-cell lymphoma may require immunohistochemical investigation the criteria of which are suggested.
  • [MeSH-major] Antigens, CD / metabolism. Biomarkers, Tumor / metabolism. Lymphoma, Large-Cell, Anaplastic / diagnosis. Lymphoma, Large-Cell, Anaplastic / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. Diagnosis, Differential. Female. Humans. Infant. Male. Middle Aged

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  • (PMID = 16405012.001).
  • [ISSN] 0004-1955
  • [Journal-full-title] Arkhiv patologii
  • [ISO-abbreviation] Arkh. Patol.
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Biomarkers, Tumor
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72. Buxton D, Bacchi CE, Gualco G, Weiss LM, Zuppan CW, Rowsell EH, Huang Q, Wang J: Frequent expression of CD99 in anaplastic large cell lymphoma: a clinicopathologic and immunohistochemical study of 160 cases. Am J Clin Pathol; 2009 Apr;131(4):574-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Frequent expression of CD99 in anaplastic large cell lymphoma: a clinicopathologic and immunohistochemical study of 160 cases.
  • By using conventional paraffin immunoperoxidase staining and tissue microarrays, we retrospectively investigated CD99 expression in a series of 160 anaplastic large cell lymphoma (ALCL) cases.
  • Of the 160 cases, 103 (64.4%) were positive for CD99.
  • CD99 expression was present in 96 (64.4%) of 149 of the common type, 4 (80%) of 5 of the small cell variant, and 3 (50%) of 6 of the lymphohistiocytic variant cases.
  • CD99 expression was slightly more frequent in anaplastic large cell lymphoma kinase (ALK)+ cases compared with ALK- cases (43/54 [80%] vs 44/81 [54%]).
  • With 2 exceptions, ALK+ ALCL was seen only in patients younger than 41 years.
  • We conclude that CD99 is frequently expressed in ALCL, with a slightly increased frequency in the younger age ALK+ cases.
  • Nodal and extranodal ALCL should be considered in the differential diagnosis when a CD99+ neoplasm is encountered.
  • [MeSH-major] Antigens, CD / biosynthesis. Biomarkers, Tumor / analysis. Cell Adhesion Molecules / biosynthesis. Lymphoma, Large-Cell, Anaplastic / metabolism

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  • (PMID = 19289593.001).
  • [ISSN] 1943-7722
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Biomarkers, Tumor; 0 / CD99 protein, human; 0 / Cell Adhesion Molecules; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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73. Engsig FN, Møller MB, Hasselbalch HK, Mahdi B, Obel N: Extreme neutrophil granulocytosis in a patient with anaplastic large cell lymphoma of T-cell lineage. APMIS; 2007 Jun;115(6):778-83
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Extreme neutrophil granulocytosis in a patient with anaplastic large cell lymphoma of T-cell lineage.
  • All microbiology tests and test for autoimmune disease were negative.
  • Conventional pathological examination of bone marrow and lymph node biopsies did not demonstrate malignant cells and inflammatory disease was suspected.
  • Immunohistochemistry and cytogenetics postmortem led to a diagnosis of anaplastic large cell lymphoma (ALCL) of T-cell lineage.
  • Involvement of peripheral blood with leukemoid reaction is a rare manifestation of ALCL.
  • [MeSH-major] Granulocytes / pathology. Lymphoma, Large-Cell, Anaplastic / pathology. Neutrophils / pathology

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  • (PMID = 17550390.001).
  • [ISSN] 0903-4641
  • [Journal-full-title] APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
  • [ISO-abbreviation] APMIS
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
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74. Guerra J, Echevarria-Escudero M, Barrio N, Velez-Rosario R: Primary endobronchial anaplastic large cell lymphoma in a pediatric patient. P R Health Sci J; 2006 Jun;25(2):159-61
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary endobronchial anaplastic large cell lymphoma in a pediatric patient.
  • A biopsy of the lesion demonstrated an anaplastic large cell lymphoma (ALCL).
  • Evaluation for disseminated disease was negative.
  • Although extranodal involvement of ALCL is frequent at some stage of the disease, endobronchial involvement is extremely rare even in the presence of advanced disease.
  • To our knowledge, this is the first primary isolated endobronchial ALCL described in a pediatric patient.
  • [MeSH-major] Bronchial Neoplasms. Lymphoma, Large B-Cell, Diffuse

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  • Hazardous Substances Data Bank. DOXORUBICIN .
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  • (PMID = 17203715.001).
  • [ISSN] 0738-0658
  • [Journal-full-title] Puerto Rico health sciences journal
  • [ISO-abbreviation] P R Health Sci J
  • [Language] eng
  • [Publication-type] Case Reports; Comparative Study; Journal Article
  • [Publication-country] Puerto Rico
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents, Hormonal; 0 / Antineoplastic Agents, Phytogenic; 0 / Immunosuppressive Agents; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; E7WED276I5 / 6-Mercaptopurine; VB0R961HZT / Prednisone; YL5FZ2Y5U1 / Methotrexate
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75. Hukin J, Davey A, Wong P, Hendson G, Aquino-Parsons C, Wu J, Sargent M: Asynchronous burst-suppression in a child with callosal Ki-1 anaplastic large cell lymphoma. Neurology; 2005 Sep 27;65(6):947-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Asynchronous burst-suppression in a child with callosal Ki-1 anaplastic large cell lymphoma.
  • A 13-year-old girl with Ki-1 anaplastic large cell lymphoma (Ki-1ALCL) bulky deposits in the brain developed raised intracranial pressure and coma associated with asynchronous burst-suppression following standard dose cranial irradiation.
  • [MeSH-major] Brain Neoplasms / complications. Coma / drug therapy. Coma / etiology. Lymphoma, Large-Cell, Anaplastic / complications. Radiotherapy / adverse effects. Substance Withdrawal Syndrome / complications


76. Recavarren RA, Yang J: Cytomorphologic features of primary anaplastic large cell lymphoma of the psoas muscle: a case report and literature review. Diagn Cytopathol; 2010 Mar;38(3):208-12
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytomorphologic features of primary anaplastic large cell lymphoma of the psoas muscle: a case report and literature review.
  • Ki-1 (CD30) positive anaplastic large cell lymphoma (ALCL) is an uncommon malignancy, which may present with nodal as well as extra-nodal disease.
  • Primary skeletal muscle Ki-1 (CD30) positive ALCL is an even rarer event with few cases reported in the literature and only some with published cytomorphologic features.
  • Smears demonstrated a predominantly discohesive population of large pleomorphic cells.
  • Morphologic and immunohistochemical features later revealed a primary psoas muscle Ki-1 (CD30) positive ALCL with negative staining for anaplastic large cell lymphoma kinase (ALK).
  • Cytologic features of ALCL mimic epithelial neoplasms, sarcomas, melanoma and other lymphomas.
  • Although rare, ALCL should be a diagnostic consideration when discohesive pleomorphic malignant cells are encountered on FNA of a muscle neoplasm.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / pathology. Muscle Neoplasms / pathology. Psoas Muscles / pathology
  • [MeSH-minor] Aged, 80 and over. Antigens, CD30 / metabolism. Biomarkers, Tumor / metabolism. Biopsy, Fine-Needle. Carcinoma / diagnosis. Cell Nucleus / metabolism. Cell Nucleus / pathology. Diagnosis, Differential. Female. Humans. Melanoma / diagnosis. Melanoma / secondary. Protein-Tyrosine Kinases / metabolism. Receptor Protein-Tyrosine Kinases. Skin Neoplasms / diagnosis

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  • (PMID = 19760764.001).
  • [ISSN] 1097-0339
  • [Journal-full-title] Diagnostic cytopathology
  • [ISO-abbreviation] Diagn. Cytopathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Biomarkers, Tumor; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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77. Li HL, Jiang HY, Ji TH, Chu HJ, Liu F, Chen XY, Wang X, Zhang G, Zhao T: [Nuclear microarray combined with fluorescence in situ hybridization for detecting ALK gene translocation in paraffin-embedded anaplastic large cell lymphoma and its significance]. Nan Fang Yi Ke Da Xue Xue Bao; 2008 Apr;28(4):572-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Nuclear microarray combined with fluorescence in situ hybridization for detecting ALK gene translocation in paraffin-embedded anaplastic large cell lymphoma and its significance].
  • OBJECTIVE: To compare the efficacy of nuclear microarray combined with fluorescence in situ hybridization (FISH) and immunohistochemistry in detecting ALK gene translocation and ALK fusion protein in anaplastic large cell lymphoma (ALCL).
  • METHODS: ALK gene translocation and ALK fusion protein in 17 paraffin-embedded ALCL specimens were detected using nuclear microarray combined with FISH and immunohistochemical straining, respectively.
  • RESULTS: The expression of ALK fusion protein was detected immunohistochemically with ALK antibody in 8 of the 17 specimens of systemic ALCL, including 4 with both nuclear and cytoplasmic positivity and 4 with only cytoplasmic positivity.
  • Dual-color FISH identified 6 positive specimens, including the 4 specimens with both nuclear and cytoplasmic positivity as identified immunohistochemically, and 2 with immunohistochemical cytoplasmic positivity.
  • [MeSH-major] In Situ Hybridization, Fluorescence / methods. Lymphoma, Large-Cell, Anaplastic / genetics. Protein-Tyrosine Kinases / genetics. Translocation, Genetic

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  • (PMID = 18495593.001).
  • [ISSN] 1673-4254
  • [Journal-full-title] Nan fang yi ke da xue xue bao = Journal of Southern Medical University
  • [ISO-abbreviation] Nan Fang Yi Ke Da Xue Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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78. Yamamoto R, Nishikori M, Tashima M, Sakai T, Ichinohe T, Takaori-Kondo A, Ohmori K, Uchiyama T: B7-H1 expression is regulated by MEK/ERK signaling pathway in anaplastic large cell lymphoma and Hodgkin lymphoma. Cancer Sci; 2009 Nov;100(11):2093-100
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] B7-H1 expression is regulated by MEK/ERK signaling pathway in anaplastic large cell lymphoma and Hodgkin lymphoma.
  • We examined B7-H1 expression in anaplastic large cell lymphoma (ALCL) and Hodgkin lymphoma (HL) and found that it was constitutively expressed in both clinical samples and cell lines.
  • In anaplastic lymphoma kinase-positive (ALK(+)) ALCL cells, B7-H1 expression was suppressed by the blocking of extracellular signal-regulated kinase (ERK) signaling and upregulated by the augmentation of ERK activity by phorbol 13-myristate 12-acetate stimulation, suggesting that B7-H1 expression is regulated by ERK signaling pathway in ALCL.
  • ERK is one of the downstream mediators of nucleophosmin (NPM)/ALK signaling in ALK(+)ALCL, and pharmacological inhibition of ALK was shown to dephosphorylate ERK and down-regulate B7-H1.
  • The involvement of NPM/ALK in B7-H1 expression was also demonstrated by introducing the construct into human non-ALCL lymphoid cell lines, which resulted in B7-H1 expression.
  • These results suggest that B7-H1 expression is controlled by common ERK signaling pathways in ALCL and HL cells.
  • [MeSH-major] Antigens, CD / analysis. Extracellular Signal-Regulated MAP Kinases / physiology. Hodgkin Disease / metabolism. Lymphoma, Large-Cell, Anaplastic / metabolism. MAP Kinase Signaling System / physiology. Mitogen-Activated Protein Kinase Kinases / physiology
  • [MeSH-minor] Antigens, CD274. Cell Line, Tumor. Humans. Protein-Tyrosine Kinases / physiology. STAT3 Transcription Factor / physiology


79. Song HH, Baik GH, Kwon JH, Lee KS, Choi YH, Choi KC, Park YE: A case of primary gastric CD30-positive anaplastic large-cell lymphoma. J Korean Med Sci; 2005 Dec;20(6):1062-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A case of primary gastric CD30-positive anaplastic large-cell lymphoma.
  • Gastric CD30-positive anaplastic large-cell lymphoma is a very rare disease.
  • We report here on a case of primary gastric anaplastic large-cell lymphoma.
  • The gross finding of the resected stomach was an 8 x 4.5 cm sized ulceroinfiltrative lesion at the pyloric antrum along the lesser curvature.
  • The microscopic examination revealed diffuse and solid proliferations of large atypical cells with pleomorphic nuclei.
  • Immunohistochemically, the tumor cells were positive for CD30, vimentin and CD3, and this was a finding compatible with anaplastic large-cell lymphoma.
  • [MeSH-major] Antigens, CD30 / metabolism. Lymphoma, Large B-Cell, Diffuse / immunology. Lymphoma, Large B-Cell, Diffuse / pathology. Stomach Neoplasms / immunology. Stomach Neoplasms / pathology

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  • (PMID = 16361823.001).
  • [ISSN] 1011-8934
  • [Journal-full-title] Journal of Korean medical science
  • [ISO-abbreviation] J. Korean Med. Sci.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Antigens, CD30; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Other-IDs] NLM/ PMC2779310
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80. Galietta A, Gunby RH, Redaelli S, Stano P, Carniti C, Bachi A, Tucker PW, Tartari CJ, Huang CJ, Colombo E, Pulford K, Puttini M, Piazza RG, Ruchatz H, Villa A, Donella-Deana A, Marin O, Perrotti D, Gambacorti-Passerini C: NPM/ALK binds and phosphorylates the RNA/DNA-binding protein PSF in anaplastic large-cell lymphoma. Blood; 2007 Oct 1;110(7):2600-9
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  • [Title] NPM/ALK binds and phosphorylates the RNA/DNA-binding protein PSF in anaplastic large-cell lymphoma.
  • The oncogenic fusion tyrosine kinase nucleophosmin/anaplastic lymphoma kinase (NPM/ALK) induces cellular transformation in anaplastic large-cell lymphomas (ALCLs) carrying the t(2;5) chromosomal translocation.
  • The interaction between NPM/ALK and PSF was dependent on an active ALK kinase domain and PSF was found to be tyrosine-phosphorylated in NPM/ALK-expressing cell lines and in primary ALK(+) ALCL samples.

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  • (PMID = 17537995.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA092318; United States / NCI NIH HHS / CA / R01 CA095512; United States / NCI NIH HHS / CA / CA095512; United States / NCI NIH HHS / CA / CA92318
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / PTB-associated splicing factor; 0 / RNA-Binding Proteins; 21820-51-9 / Phosphotyrosine; 63231-63-0 / RNA; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases
  • [Other-IDs] NLM/ PMC1988934
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81. Staber PB, Noehammer C, Dürkop H, Schauer S, Kenner L, Linkesch W, Hoefler G: mRNA expression patterns indicate CD30 mediated activation of different apoptosis pathways in anaplastic large cell lymphoma but not in Hodgkin's lymphoma. Leuk Res; 2006 Mar;30(3):343-8
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  • [Title] mRNA expression patterns indicate CD30 mediated activation of different apoptosis pathways in anaplastic large cell lymphoma but not in Hodgkin's lymphoma.
  • CD30, a member of the TNFR superfamily is overexpressed in highly proliferating tumors such as anaplastic large cell lymphoma (ALCL) and Hodgkin's lymphoma (HL).
  • CD30 stimulation leads to apoptosis and growth arrest in cultured ALCL, but not in Hodgkin-Reed-Sternberg cells.
  • To identify changes in the transcriptional program responsible for these opposing effects, we performed gene expression analysis in CD30-stimulated ALCL (Karpas 299) and HL (KM-H2) cell lines using cDNA microarrays.
  • Hierarchical clustering was applied to the whole dataset and separated the cell lines clearly with respect to their origin.
  • In HL, there were only minor CD30-specific alterations, whereas ALCL unequivocally showed a pronounced CD30-specific transcriptional response.
  • Ninety-three genes (6.6% of total) were deregulated by more than a factor of two after CD30 stimulation in ALCL cells.
  • The majority of genes identified are involved in cell cycle regulation and apoptosis. mRNA expression patterns further indicate that in contrast to HL, CD30 stimulation in ALCL induces cell death via the CD95-CD95 ligand (CD95L) pathway and the TNF-R1/TNF-R2 crosstalk.
  • These data provide a detailed view on the transcriptional changes upon CD30 stimulation and may explain the observed functional differences of HL and ALCL.
  • [MeSH-major] Antigens, CD30. Apoptosis / genetics. Cell Cycle / genetics. Gene Expression Regulation, Leukemic. Lymphoma, Large B-Cell, Diffuse / genetics. Signal Transduction
  • [MeSH-minor] Cell Line, Tumor. Gene Expression Profiling. Hodgkin Disease / genetics. Hodgkin Disease / metabolism. Humans. Oligonucleotide Array Sequence Analysis

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  • (PMID = 16198418.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD30
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82. Takahashi D, Nagatoshi Y, Nagayama J, Inagaki J, Itonoaga N, Takeshita M, Okamura J: Anaplastic large cell lymphoma in leukemic presentation: a case report and a review of the literature. J Pediatr Hematol Oncol; 2008 Sep;30(9):696-700
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  • [Title] Anaplastic large cell lymphoma in leukemic presentation: a case report and a review of the literature.
  • It is extremely rare that a patient with anaplastic large cell lymphoma (ALCL) demonstrates circulating lymphoma cells.
  • The white cell count was 26.2x10(9)/L with 95% of abnormal lymphoid cells, which were small to medium-sized with a high nucleus/cytoplasm ratio, basophilic cytoplasm, condensed nuclear chromatins, and 1 or 2 distinct nucleoli, hemoglobin 6.4 g/dL, and platelet 0.9x10(9)/L.
  • A flow cytometric analysis of abnormal cells in both the peripheral blood and bone marrow samples was strongly positive for CD30 on their cell membranes.
  • Reverse transcriptase-polymerase chain reaction of peripheral blood cell-derived mRNA also indicated the fusion gene product of anaplastic lymphoma kinase and nucleophosmin.
  • Subsequently, the patient was diagnosed to have ALCL with a rare clinical feature of a peripheral leukemic presentation, and his disease revealed to be refractory to chemotherapy.
  • On the basis of the 11 childhood cases of ALCL with leukemic presentation so far published and reviewed herein, the prognosis is very poor.
  • [MeSH-major] Leukemia / diagnosis. Lymphoma, Large-Cell, Anaplastic / pathology
  • [MeSH-minor] Antigens, CD30 / analysis. Bone Marrow Examination. Child. Fatal Outcome. Humans. Male. Protein-Tyrosine Kinases. Translocation, Genetic

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  • (PMID = 18776764.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD30; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases
  • [Number-of-references] 25
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83. Kolonić SO, Prasek-Kudrna K, Roso V, Radić-Kristo D, Planinc-Peraica A, Dzebro S, Kardum-Skelin I, Jaksić B: Value of fine-needle aspiration cytology in diagnosis of Hodgkin's lymphoma and anaplastic large cell lymphoma: one centre experience. Coll Antropol; 2010 Mar;34(1):75-9
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  • [Title] Value of fine-needle aspiration cytology in diagnosis of Hodgkin's lymphoma and anaplastic large cell lymphoma: one centre experience.
  • The aim of the study was to determine the value and limitations of cytology in diagnosis of Hodgkin's lymphoma (HL) and anaplastic large cell lymphoma (ALCL) as well as differentiation between these two entities.
  • We analysed the FNA cytodiagnoses and histopathological reports, as well as treatment and survival in 89 newly diagnosed consecutive patients with these lymphomas treated in our clinical department.
  • Cytology revealed 65 classic HL, 18 ALCL and three patients in which diagnosis was not informative.
  • Among 65 FNA cytodiagnoses of HL, comparison with histopathology was made in 61 cases and the histopathological diagnoses were as follows: 56 (91.8%) HL; three ALCL; one diffuse large B cell lymphoma and one marginal zone B cell lymphoma.
  • In the group of 18 FNA cytodiagnoses of ALCL eight patients (53.3%) had definitive diagnosis of ALCL (either as T-cell or O type), five (33.3%) of HL and in three cases a histopathological diagnosis could not be made.
  • These results confirm the value of FNA in diagnostic procedure in patients with HL and ALCL, especially in HL group of patients.
  • Since we have an almost uniform group of patients according to therapeutic approach, we did univariate analyses and found out that patients with FNA cytodiagnoses of HL, younger than 55 years, with early stage of the disease and without B symptoms had significantly longer overall survival (OS).
  • FNA cytodiagnosis has clinical relevance in differentiation between HL and ALCL.
  • [MeSH-major] Biopsy, Fine-Needle / standards. Hodgkin Disease / mortality. Hodgkin Disease / pathology. Lymphoma, Large-Cell, Anaplastic / mortality. Lymphoma, Large-Cell, Anaplastic / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Female. Humans. Lymphoma, Large B-Cell, Diffuse / mortality. Lymphoma, Large B-Cell, Diffuse / pathology. Male. Middle Aged. Reproducibility of Results. Survival Analysis. Young Adult

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  • (PMID = 20432736.001).
  • [ISSN] 0350-6134
  • [Journal-full-title] Collegium antropologicum
  • [ISO-abbreviation] Coll Antropol
  • [Language] eng
  • [Publication-type] Journal Article; Validation Studies
  • [Publication-country] Croatia
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84. Nishikori M, Ohno H, Haga H, Uchiyama T: Stimulation of CD30 in anaplastic large cell lymphoma leads to production of nuclear factor-kappaB p52, which is associated with hyperphosphorylated Bcl-3. Cancer Sci; 2005 Aug;96(8):487-97
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  • [Title] Stimulation of CD30 in anaplastic large cell lymphoma leads to production of nuclear factor-kappaB p52, which is associated with hyperphosphorylated Bcl-3.
  • Anaplastic large cell lymphoma (ALCL) and Hodgkin lymphoma (HL) express CD30 at high levels, but stimulation of this molecule has been reported to induce contradictory effects.
  • To elucidate the molecular mechanism of CD30-mediated apoptosis of ALCL, we compared the gene expression profiles of t(2;5)(p23;q35)-positive ALCL with those of HL altered by CD30 agonistic stimulation.
  • The results showed that BCL3, the high-level expression of which in ALCL was previously reported, was further upregulated in response to CD30 stimulation, along with several pro-apoptotic genes.
  • Bcl-3 protein was present as an intermediate phospho-form in the resting-state ALCL, becoming hyperphosphorylated (Bcl-3P) upon stimulation.
  • We next found that the stimulation promoted de novo synthesis of the nuclear factor (NF)-kappaB2/p100 precursor as well as processing to p52, and a series of immunoprecipitation and western blotting analyses consistently showed association of Bcl-3P with p52 in CD30-stimulated ALCL.
  • An electrophoretic mobility shift assay revealed the induction of kappaB binding activity of the p52 homodimer, and nuclear colocalization of Bcl-3 and p52 was demonstrated in anaplastic lymphoma kinase-positive ALCL tumor tissues by immunohistochemistry.
  • As Bcl-3 can act as an anti-repressor or transactivator or both, we propose that the (p52)2/Bcl-3P ternary complex, which is specifically induced in CD30-stimulated ALCL, can modulate expression of apoptosis-related genes regulated by NF-kappaB, thereby accounting for CD30-mediated apoptosis of ALCL.
  • [MeSH-major] Antigens, CD30 / genetics. Carcinoma / genetics. Lymphoma, Large B-Cell, Diffuse / genetics. NF-kappa B / genetics. Proto-Oncogene Proteins / metabolism
  • [MeSH-minor] Cell Line, Tumor. Chromosomes, Human, Pair 2. Chromosomes, Human, Pair 5. Humans. NF-kappa B p52 Subunit. Phosphorylation. Transcription Factors. Translocation, Genetic


85. Khor TS, Alessandri AJ, Jevon GP: Infant anaplastic large cell lymphoma with hemophagocytic syndrome. Pediatr Dev Pathol; 2010 Jan-Feb;13(1):72-6
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  • [Title] Infant anaplastic large cell lymphoma with hemophagocytic syndrome.
  • Anaplastic large cell lymphoma (ALCL), anaplastic lymphoma kinase (ALK)-positive, is uncommon in infancy.
  • We present an unusual occurrence of infant ALCL, ALK-positive, associated with hemophagocytic syndrome.
  • To the best of our knowledge, there have been no cases of infant ALCL, ALK-positive, described that have been associated with hemophagocytic syndrome.
  • [MeSH-major] Lymphohistiocytosis, Hemophagocytic / pathology. Lymphoma, Large-Cell, Anaplastic / pathology
  • [MeSH-minor] Antigens, CD30 / metabolism. Biomarkers, Tumor / metabolism. Chromosomes, Human, Pair 2. Failure to Thrive. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Infant. Lymph Nodes / pathology. Male. Protein-Tyrosine Kinases / metabolism. Receptor Protein-Tyrosine Kinases. Translocation, Genetic

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  • (PMID = 19863446.001).
  • [ISSN] 1093-5266
  • [Journal-full-title] Pediatric and developmental pathology : the official journal of the Society for Pediatric Pathology and the Paediatric Pathology Society
  • [ISO-abbreviation] Pediatr. Dev. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Biomarkers, Tumor; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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86. Asha LK, Thomas D, Binitha MP, Nandakumar G: Primary cutaneous multifocal CD30+ anaplastic large cell lymphoma. Indian J Dermatol Venereol Leprol; 2006 Sep-Oct;72(5):376-8
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  • [Title] Primary cutaneous multifocal CD30+ anaplastic large cell lymphoma.
  • Biopsy and immunophenotyping revealed CD 30+ anaplastic primary cutaneous large cell lymphoma.
  • Primary cutaneous anaplastic large cell lymphoma is characterized by single or grouped reddish-brown tumor nodules, which frequently tend to ulcerate.
  • [MeSH-major] Antigens, CD30 / biosynthesis. Lymphoma, Large B-Cell, Diffuse / diagnosis. Lymphoma, Large B-Cell, Diffuse / immunology. Skin Neoplasms / diagnosis. Skin Neoplasms / immunology

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  • (PMID = 17050936.001).
  • [ISSN] 0973-3922
  • [Journal-full-title] Indian journal of dermatology, venereology and leprology
  • [ISO-abbreviation] Indian J Dermatol Venereol Leprol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Antigens, CD30; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; CHOP protocol
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87. Muzzafar T, Wei EX, Lin P, Medeiros LJ, Jorgensen JL: Flow cytometric immunophenotyping of anaplastic large cell lymphoma. Arch Pathol Lab Med; 2009 Jan;133(1):49-56
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  • [Title] Flow cytometric immunophenotyping of anaplastic large cell lymphoma.
  • CONTEXT: Anaplastic large cell lymphoma (ALCL) is usually diagnosed by histologic and immunohistochemical analysis.
  • OBJECTIVE: To review our experience using flow-cytometric immunophenotyping to assess cases of ALCL and to evaluate the diagnostic utility of this technique.
  • DESIGN: Each case of ALCL was assessed by flow cytometry with 3-color or 4-color antibody panels, and data were reanalyzed by cluster analysis using Paint-a-Gate for cases with retrievable flow cytometry data files.
  • Anaplastic lymphoma kinase (ALK) was assessed by using immunohistochemistry.
  • RESULTS: Twenty-three ALCL cases were analyzed by flow cytometry.
  • In the remaining 19 cases (11 ALK(+), 8 ALK(-)), all were positive for CD30 and CD45.
  • Anaplastic large cell lymphoma cells were large and usually CD45 bright, with many or most cells falling in the region of monocytes on the CD45/side scatter plot.
  • The frequencies of T-cell antigen expression in ALK(+) cases were CD2, 67%; CD7, 60%; CD3, 45%; CD4, 33%; CD5, 14%; and CD8, 14%.
  • In ALK(-) cases, the frequencies of the T-cell antigen expression were CD2, 100%; CD3, 50%; CD4, 40%; CD7, 40%; CD5, 25%; and CD8, 20%.
  • CONCLUSIONS: Flow cytometry can be used to immunophenotype ALCL cases.
  • [MeSH-major] Flow Cytometry / methods. Immunophenotyping / methods. Lymphoma, Large-Cell, Anaplastic / diagnosis
  • [MeSH-minor] Adult. Aged. Antigens, CD / metabolism. Biopsy, Fine-Needle. Female. Humans. Immunohistochemistry. Male. Middle Aged. Protein-Tyrosine Kinases / metabolism. Receptor Protein-Tyrosine Kinases

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  • (PMID = 19123736.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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88. Eckerle S, Brune V, Döring C, Tiacci E, Bohle V, Sundström C, Kodet R, Paulli M, Falini B, Klapper W, Chaubert AB, Willenbrock K, Metzler D, Bräuninger A, Küppers R, Hansmann ML: Gene expression profiling of isolated tumour cells from anaplastic large cell lymphomas: insights into its cellular origin, pathogenesis and relation to Hodgkin lymphoma. Leukemia; 2009 Nov;23(11):2129-38
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  • [Title] Gene expression profiling of isolated tumour cells from anaplastic large cell lymphomas: insights into its cellular origin, pathogenesis and relation to Hodgkin lymphoma.
  • Anaplastic large cell lymphoma (ALCL) is a main type of T-cell lymphomas and comprises three distinct entities: systemic anaplastic lymphoma kinase (ALK) positive, systemic ALK(-) and cutaneous ALK(-) ALCL (cALCL).
  • Little is known about their pathogenesis and their cellular origin, and morphological and immunophenotypical overlap exists between ALK(-) ALCL and classical Hodgkin lymphoma (cHL).
  • We conducted gene expression profiling of microdissected lymphoma cells of five ALK(+) and four ALK(-) systemic ALCL, seven cALCL and sixteen cHL, and of eight subsets of normal T and NK cells.
  • The analysis supports a derivation of ALCL from activated T cells, but the lymphoma cells acquired a gene expression pattern hampering an assignment to a CD4(+), CD8(+) or CD30(+) T-cell origin.
  • Indeed, ALCL display a down-modulation of many T-cell characteristic molecules.
  • All ALCL types show significant expression of NFkappaB target genes and upregulation of genes involved in oncogenesis (e.g. EZH2).
  • Surprisingly, few genes are differentially expressed between systemic and cALCL despite their different clinical behaviour, and between ALK(-) ALCL and cHL despite their different cellular origin.
  • ALK(+) ALCL are characterized by expression of genes regulated by pathways constitutively activated by ALK.
  • This study provides multiple novel insights into the molecular biology and pathogenesis of ALCL.
  • [MeSH-major] Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Hodgkin Disease / genetics. Lymphoma, Large-Cell, Anaplastic / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Cell Line. Female. Humans. Immunohistochemistry. Killer Cells, Natural / cytology. Killer Cells, Natural / physiology. Male. Microdissection. Middle Aged. NF-kappa B / metabolism. Phenotype. Protein-Tyrosine Kinases / genetics. Receptor Protein-Tyrosine Kinases. Reverse Transcriptase Polymerase Chain Reaction. T-Lymphocytes / cytology. T-Lymphocytes / physiology. Young Adult

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  • (PMID = 19657361.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / NF-kappa B; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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89. Cheng M, Ott GR: Anaplastic lymphoma kinase as a therapeutic target in anaplastic large cell lymphoma, non-small cell lung cancer and neuroblastoma. Anticancer Agents Med Chem; 2010 Mar;10(3):236-49
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  • [Title] Anaplastic lymphoma kinase as a therapeutic target in anaplastic large cell lymphoma, non-small cell lung cancer and neuroblastoma.
  • Anaplastic lymphoma kinase (ALK), a receptor tyrosine kinase in the insulin receptor superfamily, was originally identified as the oncogenic NPM (nucleophosmin)-ALK fusion protein due to a t (2;5) chromosomal translocation in anaplastic large cell lymphomas.
  • The recent reports of EML4 (echinoderm microtubule-associated protein-like 4)-ALK oncogenic proteins in non-small cell lung cancer (NSCLC) and the identification of ALK activating point mutations and gene amplification in neuroblastoma have indicated ALK as a potential major therapeutic target for human cancers.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy. Lymphoma, Large-Cell, Anaplastic / drug therapy. Neuroblastoma / drug therapy. Protein-Tyrosine Kinases / antagonists & inhibitors


90. Piva R, Pellegrino E, Inghirami G: Identification and validation of the anaplastic large cell lymphoma signature. Adv Exp Med Biol; 2007;604:129-36
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification and validation of the anaplastic large cell lymphoma signature.
  • Anaplastic large cell lymphomas (ALCL) represent a subset of lymphomas in which the anaplastic lymphoma kinase (ALK) gene is fused to several partners, most frequently to the NPM gene.
  • We have previously demonstrated that the constitutive expression and phosphorylation of ALK chimeric proteins is sufficient for cellular transformation, and its activity is strictly required for the survival of ALCL cells.
  • To unravel signaling pathways required for NPM-ALK-mediated transformation and tumor maintenance, we analyzed the transcriptomes of ALK positive ALCL cell lines through experimentally controlled approaches in which ALK signaling was abrogated by an inducible ALKshRNA or by ALK inhibitors.
  • A functional RNAi screening identified new ALK transcriptional targets instrumental to cell transformation and/or to sustain the growth and survival of ALK positive ALCL cells.
  • [MeSH-major] Gene Expression Regulation. Gene Expression Regulation, Neoplastic. Lymphoma, Large B-Cell, Diffuse / diagnosis. Lymphoma, Large B-Cell, Diffuse / genetics

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  • (PMID = 17695725.001).
  • [ISSN] 0065-2598
  • [Journal-full-title] Advances in experimental medicine and biology
  • [ISO-abbreviation] Adv. Exp. Med. Biol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01-CA64033
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger
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91. Kneile JR, Tan G, Suster S, Wakely PE Jr: Expression of CD30 (Ber-H2) in nasopharyngeal carcinoma, undifferentiated type and lymphoepithelioma-like carcinoma. A comparison study with anaplastic large cell lymphoma. Histopathology; 2006 Jun;48(7):855-61
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  • [Title] Expression of CD30 (Ber-H2) in nasopharyngeal carcinoma, undifferentiated type and lymphoepithelioma-like carcinoma. A comparison study with anaplastic large cell lymphoma.
  • AIMS: Undifferentiated nasopharyngeal non-keratinizing carcinoma (UNPC), formerly known as lymphoepithelioma, frequently metastasizes at an early stage to regional lymph nodes and, thus, may be difficult to distinguish from Hodgkin's lymphoma (HL) or anaplastic large cell lymphoma (ALCL).
  • CD30 expression is a useful diagnostic stain in both HL and ALCL, but its expression in UNPC deserves clarification.
  • The aim of this study was to evaluate CD30 expression in UNPC and lymphoepithelioma-like carcinoma (LELC) from other anatomic locations and compare it with ALCL and squamous cell carcinoma (SCC).
  • METHODS AND RESULTS: CD30 immunoreactivity was examined in 38 cases of primary or metastatic UNPC, six cases of LELC, 10 cases of SCC and seven cases of ALCL.
  • CD30 immunoreactivity was observed in four of 38 (10.5%) cases of UNPC.
  • CD30 staining was absent in all cases of LELC (0/6) and SCC (0/10).
  • All cases of ALCL (7/7) were strongly positive for CD30.
  • CONCLUSIONS: The majority of cases of UNPC are immunohistochemically negative for CD30; however, a small subset of cases expresses CD30 antigen.
  • These findings provide additional evidence that CD30 expression is not restricted to neoplasms of lymphoid origin.
  • This should be taken into consideration when interpreting CD30 immunohistology and the possibility of UNPC.
  • [MeSH-major] Antigens, CD30 / biosynthesis. Carcinoma / pathology. Carcinoma, Squamous Cell / pathology. Lymphoma, Large-Cell, Anaplastic / pathology. Nasopharyngeal Neoplasms / pathology


92. Watanabe M, Sasaki M, Itoh K, Higashihara M, Umezawa K, Kadin ME, Abraham LJ, Watanabe T, Horie R: JunB induced by constitutive CD30-extracellular signal-regulated kinase 1/2 mitogen-activated protein kinase signaling activates the CD30 promoter in anaplastic large cell lymphoma and reed-sternberg cells of Hodgkin lymphoma. Cancer Res; 2005 Sep 1;65(17):7628-34
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] JunB induced by constitutive CD30-extracellular signal-regulated kinase 1/2 mitogen-activated protein kinase signaling activates the CD30 promoter in anaplastic large cell lymphoma and reed-sternberg cells of Hodgkin lymphoma.
  • High expression of CD30 and JunB is characteristic of tumor cells in anaplastic large cell lymphoma (ALCL) and Hodgkin lymphoma (HL).
  • Possible interactions of CD30 and JunB were examined in this study.
  • We found that the CD30 promoter in tumor cells of both nucleophosmin (NPM)-anaplastic lymphoma kinase (ALK)-positive and NPM-ALK-negative ALCL and HL is regulated by a constitutively active CD30-extracellular signal-regulated kinase (ERK) 1/2 mitogen-activated protein kinase (MAPK).
  • Phosphorylation of ERK1/2 MAPK was confirmed in nuclei of tumor cells in both ALCL and HL.
  • CD30-ERK1/2 MAPK signals induce JunB expression, which maintains high activity of the CD30 promoter.
  • JunB induction seems to be largely independent of nuclear factor kappaB in ALCL and HL.
  • These results show a common mechanism of CD30 overexpression in ALCL and HL, although the outcome of CD30 signaling differs between NPM-ALK-positive ALCL and NPM-ALK-negative ALCL, cutaneous ALCL, and HL as we recently reported.
  • [MeSH-major] Antigens, CD30 / metabolism. Extracellular Signal-Regulated MAP Kinases / metabolism. Hodgkin Disease / metabolism. Lymphoma, Large B-Cell, Diffuse / metabolism. MAP Kinase Signaling System / physiology. Proto-Oncogene Proteins c-jun / biosynthesis. Reed-Sternberg Cells / metabolism
  • [MeSH-minor] Cell Line, Tumor. Humans. K562 Cells. NF-kappa B / metabolism. Promoter Regions, Genetic. Protein Binding. Transcription Factor AP-1 / metabolism


93. Saito S, Yasui K, Hosoda W, Ogawa M, Kobayashi N, Sakashita K, Koike K: CD30+ anaplastic large cell lymphoma complicated by pyoderma gangrenosum with increased levels of serum cytokines. Eur J Haematol; 2006 Sep;77(3):251-4
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  • [Title] CD30+ anaplastic large cell lymphoma complicated by pyoderma gangrenosum with increased levels of serum cytokines.
  • We here present the case of a 5-yr-old girl with pyoderma gangrenosum (PG) in association with underlying CD30+ anaplastic large cell lymphoma with increased serum cytokine levels (interleukin-8, granulocyte colony-stimulating factor).
  • [MeSH-major] Cytokines / blood. Lymphoma, Large B-Cell, Diffuse / complications. Lymphoma, Large B-Cell, Diffuse / immunology. Pyoderma Gangrenosum / etiology. Pyoderma Gangrenosum / immunology
  • [MeSH-minor] Antigens, CD30 / metabolism. Child, Preschool. Female. Granulocyte Colony-Stimulating Factor / blood. Humans. Interleukin-8 / blood. Osteolysis / etiology. Osteolysis / pathology

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  • (PMID = 16923111.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Cytokines; 0 / Interleukin-8; 143011-72-7 / Granulocyte Colony-Stimulating Factor
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94. O'leary H, Savage KJ: The spectrum of peripheral T-cell lymphomas. Curr Opin Hematol; 2009 Jul;16(4):292-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The spectrum of peripheral T-cell lymphomas.
  • PURPOSE OF REVIEW: This review summarizes recent progress that has advanced our understanding of the pathobiology and prognosis of peripheral T-cell lymphomas including the changes introduced to the updated World Health Organization classification of lymphoid neoplasms.
  • RECENT FINDINGS: The International Peripheral T-Cell Lymphoma Project was a large collaborative project, highlighting the clinico-pathologic and geographic differences of this diverse group of diseases.
  • Peripheral T-cell lymphoma, not otherwise specified, is a biologically heterogeneous subtype, and a number of studies including investigations using molecular profiling have explored whether meaningful prognostic or biologic subgroups can be identified.
  • Angioimmunoblastic T-cell lymphoma demonstrates overlapping immunophenotypical and molecular features with normal follicular T-helper cells, giving some insight into the cell of origin.
  • Systemic anaplastic large cell lymphoma is composed of two disease groups based on the presence or absence of anaplastic lymphoma kinase overexpression.
  • Anaplastic lymphoma kinase-positive anaplastic large cell lymphoma has a significantly better prognosis than anaplastic lymphoma kinase-negative anaplastic large cell lymphoma and molecular studies have illustrated that each entity has a distinct molecular profile.
  • Anaplastic lymphoma kinase-negative anaplastic large cell lymphoma has been recently shown to have a more favourable, but still unsatisfactory, prognosis than peripheral T-cell lymphoma, not otherwise specified, and biological and molecular distinctions confirm that they are separate entities.
  • SUMMARY: Advances are being made in understanding the unique pathobiology of the peripheral T-cell lymphoma subtypes that will help to refine diagnoses, identify potential prognostic markers, elucidate the molecular mechanisms critical in disease pathogenesis and define new therapeutic targets in the poor-risk population.
  • [MeSH-major] Lymphoma, T-Cell, Peripheral / classification. Lymphoma, T-Cell, Peripheral / pathology
  • [MeSH-minor] Antigens, Neoplasm / genetics. Cyclin A / genetics. Cyclin B / genetics. DNA Topoisomerases, Type II / genetics. DNA-Binding Proteins / genetics. Gene Expression Profiling. Humans. Prognosis. Proliferating Cell Nuclear Antigen / genetics. Survival Analysis. World Health Organization

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  • (PMID = 19509496.001).
  • [ISSN] 1531-7048
  • [Journal-full-title] Current opinion in hematology
  • [ISO-abbreviation] Curr. Opin. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Cyclin A; 0 / Cyclin B; 0 / DNA-Binding Proteins; 0 / Proliferating Cell Nuclear Antigen; EC 5.99.1.3 / DNA Topoisomerases, Type II; EC 5.99.1.3 / DNA topoisomerase II alpha
  • [Number-of-references] 47
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95. Driss M, Abbes I, Mrad K, Sassi S, Oubich F, Barsaoui S, Romdhane KB: Primary CD30/ALK-1 positive anaplastic large cell lymphoma of the skeletal muscle in a child. Pathologica; 2009 Apr;101(2):97-100
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  • [Title] Primary CD30/ALK-1 positive anaplastic large cell lymphoma of the skeletal muscle in a child.
  • Anaplastic large cell lymphoma (ALCL) represents approximately 10 to 30% of all childhood non-Hodgkin lymphomas.
  • Biopsy of the lesion showed large anaplastic cells with voluminous and abundant cytoplasm as well as folded nuclei.
  • The tumour cells were positive for CD30, CD3, EMA and ALK-1.
  • This case emphasizes the occurrence of anaplastic large cell lymphoma in the soft tissue and the favourable outcome of ALK-positive anaplastic large cell lymphoma.
  • [MeSH-major] Activin Receptors, Type II / biosynthesis. Antigens, CD30 / biosynthesis. Lymphoma, Large-Cell, Anaplastic / pathology. Muscle Neoplasms / pathology. Muscle, Skeletal / pathology

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  • (PMID = 19886557.001).
  • [ISSN] 0031-2983
  • [Journal-full-title] Pathologica
  • [ISO-abbreviation] Pathologica
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Biomarkers, Tumor; EC 2.7.11.30 / ACVRL1 protein, human; EC 2.7.11.30 / Activin Receptors, Type II
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96. Colen CB, Rayes M, Kupsky WJ, Guthikonda M: Synchronous meningioma and anaplastic large cell lymphoma. Neuropathology; 2010 Jun;30(3):260-6
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  • [Title] Synchronous meningioma and anaplastic large cell lymphoma.
  • When they occur, most cases are associated with metastatic disease.
  • To the best of our knowledge, we report the first case of an atypical meningioma infiltrated by a T-cell-primary central nervous system lymphoma (PCNSL), specifically anaplastic large cell lymphoma (ALCL).
  • This tumor was composed of moderately large lymphoid cells with large nuclei, prominent nucleoli, and amphophilic cytoplasm.
  • These cells were strongly immunoreactive for CD3 and CD30 but remained unstained with EMA, anaplastic lymphoma kinase-1 (ALK-1), CD15 or cytotoxic associated antigen TIA-1.
  • The morphologic and immunohistochemical features were considered typical of anaplastic large T-cell lymphoma.
  • The pathogenesis of this association may have been due to radiation-mediated breakdown of the blood-brain barrier with subsequent T-cell infiltration and proliferation.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / pathology. Meningeal Neoplasms / pathology. Meningioma / pathology


97. Rekhi B, Sridhar E, Viswanathan S, Shet TM, Jambhekar NA: ALK+ anaplastic large cell lymphoma with cohesive, perivascular arrangements on cytology, mimicking a soft tissue sarcoma: a report of 2 cases. Acta Cytol; 2010 Jan-Feb;54(1):75-8
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  • [Title] ALK+ anaplastic large cell lymphoma with cohesive, perivascular arrangements on cytology, mimicking a soft tissue sarcoma: a report of 2 cases.
  • BACKGROUND: An accurate recognition of a lymphoma at an extranodal site is essential to avoid unnecessary excisions.
  • Fine needle aspiration cytology (FNAC) has been recognized as a useful tool in the primary diagnosis of soft tissue tumors.
  • An anaplastic large cell lymphoma (ALCL), occurring in soft tissues, poses a diagnostic challenge.
  • We present the cytomorphology of 2 cases of anaplastic lymphoma kinase (ALK)+ ALCL that displayed a perivascular arrangement, thereby mimicking a sarcoma.
  • Differential diagnoses included a rhabdomyosarcoma and a lymphoma.
  • On biopsy and immunohistochemistry, tumor cells were positive for vimentin, LCA, EMA, CD30 and ALK.
  • CONCLUSION: ALCL should be considered in the differential diagnosis of pediatric soft tissue tumors, especially in cases with multifocal involvement.
  • [MeSH-major] Biopsy, Fine-Needle. Lymphoma, Large-Cell, Anaplastic / metabolism. Lymphoma, Large-Cell, Anaplastic / pathology. Protein-Tyrosine Kinases / metabolism. Soft Tissue Neoplasms / pathology
  • [MeSH-minor] Adolescent. Child. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Male. Receptor Protein-Tyrosine Kinases. Sarcoma / pathology

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  • (PMID = 20306994.001).
  • [ISSN] 0001-5547
  • [Journal-full-title] Acta cytologica
  • [ISO-abbreviation] Acta Cytol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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98. Rupani A, Modi C, Desai S, Rege J: Primary anaplastic large cell lymphoma of central nervous system--a case report. J Postgrad Med; 2005 Oct-Dec;51(4):326-7
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  • [Title] Primary anaplastic large cell lymphoma of central nervous system--a case report.
  • Central nervous system (CNS) involvement is extremely rare in anaplastic large cell lymphoma (ALCL).
  • Primary ALCL of CNS on radiology is often misdiagnosed as tuberculosis.
  • We report a fatal case of primary ALCL of CNS in a 17 year old male.
  • Biopsy showed large pleomorphic cells.
  • Immunohistochemical stains showed positivity for CD30, CD43, EMA and ALK-1.
  • Hence a high level of suspicion is essential for early diagnosis and for instituting appropriate treatment.
  • [MeSH-major] Central Nervous System Neoplasms / diagnosis. Lymphoma, Large B-Cell, Diffuse / diagnosis
  • [MeSH-minor] Adolescent. Diagnostic Errors. Fatal Outcome. Humans. Magnetic Resonance Imaging. Male. Tuberculosis / diagnosis


99. Lones MA, Heerema NA, Le Beau MM, Perkins SL, Kadin ME, Kjeldsberg CR, Sposto R, Meadows A, Siegel S, Buckley J, Finlay J, Abromowitch M, Cairo MS, Sanger WG: Complex secondary chromosome abnormalities in advanced stage anaplastic large cell lymphoma of children and adolescents: a report from CCG-E08. Cancer Genet Cytogenet; 2006 Dec;171(2):89-96
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Complex secondary chromosome abnormalities in advanced stage anaplastic large cell lymphoma of children and adolescents: a report from CCG-E08.
  • Among pediatric non-Hodgkin lymphomas, one of the most distinctive types is anaplastic large cell lymphoma (ALCL).
  • Specific chromosomal abnormalities are associated with prognosis in childhood acute lymphoblastic leukemia, but chromosome abnormalities have not been evaluated for prognostic value in pediatric ALCL.
  • For Children's Cancer Group protocol CCG-E-08 Etiologic Study of Non-Hodgkin Lymphoma in Childhood, three patients were enrolled with cytogenetic analysis of ALCL and simultaneously enrolled on treatment protocol CCG-552.
  • Pathology material and karyotypes at initial diagnosis underwent central review.
  • All patients had advanced disease (stage III).
  • Disease progressed or relapsed in two patients, and one died.
  • In two patients with progressive disease or relapse, additional chromosomal abnormalities at 1q21 and 10q24, possibly involving MCL1 and HOX11/TCL3, respectively, may have contributed to worse outcome.
  • Pediatric ALCL cases frequently have complex karyotypes and usually involve ALK/NPM translocations in this limited study.
  • Additional chromosome abnormalities may be involved in the pathogenesis of ALCL.
  • Further studies are warranted in larger cohorts of children and adolescents with ALCL.
  • [MeSH-major] Chromosome Aberrations. Lymphoma, Large B-Cell, Diffuse / genetics. Lymphoma, Large B-Cell, Diffuse / pathology

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  • (PMID = 17116485.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 13539; United States / NCI NIH HHS / CA / CA 98543
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
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100. Gorgidze LA, Vorob'ev IA: [A morphometric analysis of the nuclei and nucleoli in tumor cells in lymphogranulomatosis, diffuse large B-cell lymphoma and anaplastic large cell lymphoma]. Ter Arkh; 2009;81(2):71-5
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  • [Title] [A morphometric analysis of the nuclei and nucleoli in tumor cells in lymphogranulomatosis, diffuse large B-cell lymphoma and anaplastic large cell lymphoma].
  • AIM: To make a comparative morphometric analysis of the nuclei and nucleoli of tumor cells in lymphogranulomatosis (LGM), diffuse large B-cell lymphoma (DLBCL) and anaplastic large cell lymphoma (ALCL) for differential diagnosis of these lymphomas.
  • RESULTS: Mean area of tumor cell nuclei in LGM was 97.25 +/- 68.77 mcm2, in DLBCL and ALCL--55.89 +/- 20.13 mcm2 and 70.31 +/- 34.64 mcm2, respectively.
  • Hodgkin's and Berezovsky-Rid-Sternberg cell bucleoli area was the largest (11.44 +/- 7.83 mcm2).
  • Mean area of the nucleoli in DLBCL was 3.05 +/- 1.58, in ALCL--5.53 +/- 4.94 mcm2.
  • CONCLUSION: Nucleoli in Hodgkin 's cells are significantly larger than those in the tumor cells in ALCL and DLBCL and the nucleoli with the area more than 12 mcm2 can be used in differential diagnosis between LGM and DLBCL but not between LGM and ALCL.
  • [MeSH-major] Cell Nucleolus / pathology. Cell Nucleus / pathology. Hodgkin Disease / pathology. Lymphoma, Large B-Cell, Diffuse / pathology. Lymphoma, Large-Cell, Anaplastic / pathology
  • [MeSH-minor] Biopsy. Diagnosis, Differential. Humans






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